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Kidney MCQs

Posted by Dr KAMAL DEEP on May 26, 2011

1.Glomerulosclerosis is a feature of –
a) Diabetes mellitus
b) Hypertension
c) Acute glomerular
d) Nephrotic syndrome
Ans is A
CAUSES OF NEPHROTIC SYNDROME in order of frequency-
Primary Glomerular Disease-Membranous glomerulonephritis,Lipoid nephrosis,Focal segmental glomerulosclerosis,Membranoproliferative glomerulonephritis,Other proliferative glomerulonephritis (focal, “pure mesangial,” IgA nephropathy)
Systemic Diseases–Diabetes mellitus,Amyloidosis,Systemic lupus erythematosus,Drugs (gold, penicillamine, “street heroin”),Infections (malaria, syphilis, hepatitis B, acquired immunodeficiency syndrome)
Malignant disease (carcinoma, melanoma),Miscellaneous (bee-sting allergy, hereditary nephritis)
*Approximate prevalence of primary disease = 95% in children, 60% in adults. Approximate prevalence of systemic disease = 5% in children, 40% in adults.
Diabetic Nephropathy
(See also Chapter 21 page 923 of robbins ) . The kidneys are prime targets of diabetes. Renal failure is second only to myocardial infarction as a cause of death from this disease. Three lesions are encountered: (1) glomerular lesions; (2) renal vascular lesions, principally arteriolosclerosis; and (3) pyelonephritis, including necrotizing papillitis.
The most important glomerular lesions are capillary basement membrane thickening, diffuse glomerulosclerosis, and nodular glomerulosclerosis. These are described in detail in Chapter 21 . The glomerular capillary basement membranes are thickened throughout their entire length. This change can be detected by electron microscopy within a few years of the onset of diabetes, sometimes without any associated change in renal function.
Diffuse glomerulosclerosis consists of a diffuse increase in mesangial matrix along with mesangial cell proliferation and is always associated with basement membrane thickening. It is found in most patients with disease of more than 10 years’ duration. When glomerulosclerosis becomes marked, patients manifest the nephrotic
Nodular glomerulosclerosis and the diffuse lesion are fundamentally similar lesions of the mesangium. The nodular lesion, however, is virtually pathognomonic of diabetes, so long as care is taken to exclude membranoproliferative (lobular) glomerulonephritis, the glomerulonephritis associated with light-chain disease, and amyloidosis. Approximately 15% to 30% of long-term patients with diabetes develop nodular glomerulosclerosis, and in most instances it is associated with renal failure
Nodular glomerulosclerosis describes a glomerular lesion made distinctive by ball-like deposits of a laminated matrix within the mesangial core of the lobule (see Fig. 21-32) . These nodules tend to develop in the periphery of the glomerulus, and since they arise within the mesangium, they push the glomerular capillary loops even more to the periphery. Often these capillary loops create halos about the nodule. This distinctive change has been called the Kimmelstiel-Wilson lesion, after the pioneers who described it. They usually contain trapped mesangial cells. Diffuse glomerulosclerosis is present in glomeruli not affected by nodular glomerulosclerosis.
Robbins 967 6th ed
Focal segmental glomerulosclerosis occurs in the following settings
in association with other known conditions, such as HIV infection and heroin addiction
Hypertension- Arteriolar nephrosclerosis (fibrnoid necrosis)


Kimmelstiel-wilson disease is diagnostic of
a)Diabetic glomerulosclerosis
b)Hypertension benign
c)Malignant hypertension
Already Described above–

Charactersitic feature of kidneys in diabetes mellitus is —(Al 89)
a)Nodular sclerosis
b)Fibrin cap
c)Papillary necrosis
d)Difuse glomendosclerosis
Ans is A…already described above

Nephrotic syndrome is caused by all except —
a) Malaria
b) Penicillamine
c) Syphilis
d) Shock
Ans is D
1.Acute nephritic syndrome—Hematuria, azotemia, variable proteinuria, oliguria, edema, and hypertension
2.Rapidly progressive glomerulonephritis–Acute nephritis, proteinuria, and acute renal failure
3.Nephrotic syndrome: >3.5 gm proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria
4.Chronic renal failure:Azotemia uremia progressing for years
5.Asymptomatic hematuria or proteinuria:Glomerular hematuria; subnephrotic proteinuria
CAUSES OF NEPHROTIC SYNDROME in order of frequency-
Primary Glomerular Disease-Membranous glomerulonephritis,Lipoid nephrosis,Focal segmental glomerulosclerosis,Membranoproliferative glomerulonephritis,Other proliferative glomerulonephritis (focal, “pure mesangial,” IgA nephropathy)
Systemic Diseases–Diabetes mellitus,Amyloidosis,Systemic lupus erythematosus,Drugs (gold, penicillamine, “street heroin”),Infections (malaria, syphilis, hepatitis B, acquired immunodeficiency syndrome)
Malignant disease (carcinoma, melanoma),Miscellaneous (bee-sting allergy, hereditary nephritis)
robbins 953 6th ed


Transitional cell carcinomas can be caused by —
a) Napthylamine
b) Smoking
c) Bilharziasis
d) Betel nut
Ans. Three options are correct i.e., ‘a, b & c’ {Ref : Robbin’s 7″/e p. 1029 & 6th/e p. 1007]
A number of factors have been implicated in the causation of transitional cell carcinoma. Some of the more important contributors include the following:
Cigarette smoking is clearly the most important influence, increasing the risk threefold to sevenfold, depending on the pack-years and smoking habits. Fifty per cent to 80% of all bladder cancers among men are associated with the use of cigarettes. Cigars, pipes, and smokeless tobacco invoke a much smaller risk.
Industrial exposure to arylamines, particularly 2-naphthylamine as well as related compounds, as pointed out in the earlier discussion of chemical carcinogenesis (Chapter 8) . The cancers appear 15 to 40 years after the first exposure.
Schistosoma haematobium infections in areas where these are endemic (Egypt, Sudan) are an established risk. The ova are deposited in the bladder wall and incite a brisk chronic inflammatory response that induces progressive mucosal squamous metaplasia and dysplasia and, in some instances, neoplasia. Seventy per cent of the cancers are squamous, the remainder being transitional cell carcinoma.
Long-term use of analgesics, implicated also in analgesic nephropathy (Chapter 21) .
Heavy long-term exposure to cyclophosphamide, an immunosuppressive agent, induces as noted hemorrhagic cystitis and increases the risk of bladder cancer.
How these influences induce cancer is unclear, but a number of genetic alterations have been observed in transitional cell carcinoma. The cytogenetic and molecular alterations are heterogeneous. Particularly common (occurring in 30% to 60% of tumors studied) are chromosome 9 monosomy or deletions of 9p and 9q as well as deletions of 17p, 13q, 11p, and 14q. [8] The chromosome 9 deletions are the only genetic changes present frequently in superficial papillary tumors and occasionally in noninvasive flat tumors.

IMPORTANT POINT IN TREATMENT OF TRANSITIONAL CELL CARCINOMA OF BLADDER:–Intravesical therapies are used in two general contexts: as an adjuvant to
a complete endoscopic resection to prevent recurrence or, less commonly,
to eliminate disease that cannot be controlled by endoscopic resection
alone. Intravesical treatments are advised for patients with recurrent disease,
>40% involvement of the bladder surface by tumor, diffuse CIS, or T1
disease. The standard intravesical therapy, based on randomized comparisons,
is bacillus Calmette-Guerin (BCG) in six weekly instillations, followed
by monthly maintenance administrations for ≥1 year

At least 95% of cancers of the oral cavity (including the tongue) are squamous cell carcinomas.A major regional predisposing influence is the chewing of betel nuts and pan in India and parts of Asia.
Though smoking is related to both types.

Commonest type of nephrotic syndrome seen in children
a) Focal
b) Diffuse
c) Minimal change
d) Proliferative
Ans. is ‘c’ i.e., Minimal change [Ref : Robbin’s rie p. 979 t (20.8) & 6THe p. 954]
Membranous glomerulonephritis is the most common cause of the nephrotic syndrome in adults. It is characterized by diffuse thickening of the glomerular capillary wall and the accumulation of electron-dense, immunoglobulin-containing deposits along the epithelial (subepithelial) side of the basement membrane.
Minimal Change Disease (Lipoid Nephrosis)This relatively benign disorder is the most frequent cause of nephrotic syndrome in children. It is characterized by diffuse loss of foot processes of epithelial cells in glomeruli that appear virtually normal by light microscopy. The peak incidence is between 2 and 6 years of age.

Basement membrane has type…. Collagen –
a) I
b) II
c) II
Ans. is ‘d’ i.e., IV [Ref : Robbin’s 7h/e p. 956 & 6e p. 931]
The glomerular capillary wall is the filtering membrane and consists of the following structures [2] (Fig. 21-2) :
A thin layer of fenestrated endothelial cells, each fenestrum being about 70 to 100 nm in diameter.
A glomerular basement membrane (GBM) with a thick electron-dense central layer, the lamina densa, and thinner electron-lucent peripheral layers, the lamina rara interna and lamina rara externa. The GBM consists of collagen (mostly type IV), laminin, polyanionic proteoglycans (mostly heparan sulfate), fibronectin, entactin, and several other glycoproteins. Type IV collagen forms a network suprastructure to which other glycoproteins attach. The building block (monomer) of this network is a triple-helical molecule made up of three alpha chains, composed of one or more of six types of alpha chains (alpha1 to alpha6 or COL4A1 to COL4A6), the most common consisting of alpha1 alpha2 alpha1 (Fig. 21-3) . [3] Each molecule consists of a 7S domain at the amino terminus, a triple-helical domain in the middle, and a globular noncollagenous domain (NC1) at the carboxyl terminus. The NC1 domain is important for helical formation and also for assembly of collagen monomers into dimers. The 7S domain, in turn, is involved in formation of tetramers, and thus a porous suprastructure evolves. Glycoproteins (laminin, entactin) and acidic proteoglycans (perlecan) attach to the collagenous suprastructure [4] (Fig. 21-4) . These biochemical determinants are critical to understanding glomerular diseases. For example, as we shall see, the NC1 domain is the antigenic site in anti-GBM nephritis; genetic defects in the alpha chains underlie some forms of hereditary nephritis; and the acidic porous nature of the GBM determines its permeability characteristics.
The visceral epithelial cells (podocytes), structurally complex cells that possess interdigitating processes embedded in and adherent to the lamina rara externa of the basement membrane. Adjacent foot processes (pedicels) are separated by 20- to 30-nm-wide filtration slits, which are bridged by a thin diaphragm.
The entire glomerular tuft is supported by mesangial cells lying between the capillaries. Basement membrane-like mesangial matrix forms a meshwork through which the mesangial cells are scattered. These cells, of mesenchymal origin, are contractile, phagocytic, and capable of proliferation, of laying down both matrix and collagen, and of secreting a number of biologically active mediators. They are, as we shall see, important players in many forms of human glomerulonephritis.

Bundles of banded fibers with high tensile strength
Skin (80%), bone (90%), tendons, most other organs
Thin fibrils; structural protein
Cartilage (50%), vitreous humor
Thin fibrils; pliable
Blood vessels, uterus, skin (10%)
All basement membranes
Amorphous/fine fibrils
2 – 5% of interstitial tissues, blood vessels
Amorphous/fine fibrils
Interstitial tissues
Anchoring filament
Dermal-epidermal junction
Probably amorphous
Endothelium-Descemet membrane
Possible role in maturation of cartilage

IMPORTANT—Three groups of macromolecules are physically associated to form the ECM: (1) fibrous structural proteins, such as the collagens and elastins; (2) a diverse group of adhesive glycoproteins, including fibronectin and laminin; and (3) a gel of proteoglycans and hyaluronan. These macromolecules assemble into two general organizations: interstitial matrix and BM (basal membrane). The interstitial matrix is present in spaces between epithelial, endothelial, and smooth muscle cells and in connective tissue. It consists of fibrillar (types I, III, V) and nonfibrillar collagen, elastin, fibronectin, proteoglycans, hyaluronate, and other components. BMs are produced by epithelial and mesenchymal cells and are closely associated with the cell surface. They consist of a network of amorphous nonfibrillar collagen (mostly type IV), laminin, heparan sulfate, proteoglycan, and other glycoproteins

Bilateral contracted kidney occurs in all except
a)Diabetes mellitus (AIIMS 90)
b)Benign nephrosclerosis
c)Chronic pyelonephritis
d)Chronic glomerular nephritis
Ans. is ‘a’ i.e., Diabetes mellitus [Ref : Chandrasoma taylor 3rd/e p. 725, table (49.2)]
Table 49–2. Differential Diagnosis of a Granular, Contracted Kidney.
ARE :-Chronic Glomerulonephritis Chronic Pyelonephritis Benign Nephrosclerosis (Hypertension)

Glomerulonephritis is due to:-
a)Type I hypersensitivity reaction
b)Type IV hypersensitivity reation
c)Immune complex deposition
d)Type V hypersensitivity reaction
Ans. is ‘c’ i.e., Immune complex deposition [Ref : Robbin’s 7/e p. 975 & 6th/e p. 943]
Immune-mediated glomerulonephritis (Chaps. 274 and275) accounts for a large fraction of acquired renal disease. The majority of cases are associated with the deposition of antibodies, often autoantibodies, within the glomerular tuft, indicating dysregulation of humoral immunity. Cellular immune mechanisms also contribute to the pathogenesis of antibody-mediated glomerulonephritis by modulating antibody production and through antibody-dependent cell cytotoxicity (see below). In addition, cellular immune mechanisms probably play a primary role in the pathophysiology of “pauci-immune” glomerulonephritides, notable for robust glomerular inflammation in the absence of immunoglobulin deposition.

Antiglomerular antibodies are present in —
a)Good pasture syndrome (Al 90)
b)Focal gloumerulonephritis
c)Membramcous glomerulonephritis
d)Membrano proliferative glomerulonephritis
RPGN may be caused by a number of different diseases, some restricted to the kidney and others systemic. [34] Although no single mechanism can explain all cases, there is little doubt that in most cases the glomerular injury is immunologically mediated. Thus, a practical classification divides RPGN into three groups on the basis of immunologic findings (Table 21-6) . In each group, the disease may be associated with a known disorder or it may be idiopathic.
Type I RPGN is best remembered as anti-GBM disease and hence is characterized by linear deposits of IgG and, in many cases, C3 in the GBM, as previously described. In some of these patients, the anti-GBM antibodies cross-react with pulmonary alveolar basement membranes to produce
Goodpasture syndrome
TYPE II RPGN (immune complex)
Systemic lupus erythematosus
Henoch-Schonlein purpura (IgA)
TYPE III RPGN (pauci-immune)
(ANCA associated)
Wegener granulomatosis
Microscopic polyarteritis nodosa
the clinical picture of pulmonary hemorrhages associated with renal failure ( Goodpasture syndrome). The Goodpasture antigen, as noted, resides in the noncollagenous portion of the alpha3 chain of collagen type IV. What triggers the formation of these antibodies is unclear in most patients. Exposure to viruses or hydrocarbon solvents (found in paints and dyes) has been implicated in some patients, as have various drugs and cancers. Cigarette smoking appears to play a permissive role, since most patients who develop pulmonary hemorrhage are smokers. There is a high prevalence of certain HLA subtypes and haplotypes (e.g., HLA-DRB1), a finding consistent with the genetic predisposition to autoimmunity. [34]
Type II RPGN is an immune complex- mediated disease. It can be a complication of any of the immune complex nephritides, including postinfectious glomerulonephritis, SLE, IgA nephropathy, and Henoch-Schonlein purpura. In some cases, immune complexes can be demonstrated, but the underlying cause is undetermined. In all of these cases, immunofluorescence studies reveal the characteristic (“lumpy bumpy”) granular pattern of staining. These patients cannot usually be helped by plasmapheresis, and they require treatment for the underlying disease.
Type III RPGN, also called pauci-immune type, is defined by the lack of anti-GBM antibodies or immune complexes by immunofluorescence and electron microscopy. Most of these patients have antineutrophil cytoplasmic antibody (ANCA) in the serum, which, as we have seen (Chapter 12) , plays a role in some vasculitides. Hence, in some cases, type III RPGN is a component of a systemic vasculitis such as Wegener granulomatosis or microscopic polyarteritis. In many cases, however, pauci-immune crescentic glomerulonephritis is isolated and hence idiopathic. More than 90% of such idiopathic cases have C-ANCA or P-ANCA in the sera.
To summarize, all three types of RPGN may be associated with a well-defined renal or extrarenal disease, but in many cases (approximately 50%) the disorder is idiopathic. Of the idiopathic cases, about one fourth have anti-GBM disease (RPGN type I) without lung involvement; another one fourth have type II RPGN; and the remainder are pauci-immune or type III RPGN. The common denominator in all types of RPGN is severe glomerular injury.


In crescentric glomerulonephritis, prognosis depends on —(AI 90)
a) Size
b) Cellularity
c) Number
d) Basement membrane break
Ans. is ‘c’ i.e., Number [Ref : Basic Robbin’s p. 453]
A crescent is a half-moon-shaped collection of cells in Bowman’s space, usually composed of proliferating parietal epithelial cells and infiltrating monocytes. Because crescentic glomerulonephritis is often associated with renal failure that progresses rapidly over week to months, the clinical term rapidly progressive glomerulonephritis and pathologic term crescentic glomerulonephritis are often used interchangeably

The epithelium in the ureter is —
a) Squamous
b) Columnar
c) Ciliated columnar
d) Transitional
Urothelium is a specialized epithelium that lines much of the urinary tract and prevents its rather toxic contents from damaging surrounding structures. It extends from the ends of the collecting ducts of the kidneys, through the ureters (p. 1277) and bladder (p. 1292), to the proximal portion of the urethra. In males it covers the urethra as far as the ejaculatory ducts, then becomes intermittent and is finally replaced by stratified columnar epithelium in the membranous urethra. In females it extends as far as the urogenital membrane. During development, part of it is derived from mesoderm and part from ectoderm and endoderm
The epithelium lining the preprostatic urethra and the proximal part of the prostatic urethra is a typical urothelium. It is continuous with that lining the bladder, and with the epithelium lining the ducts of the prostate and bulbourethral glands, the seminal vesicles, and the vasa deferentia and ejaculatory ducts. These relationships are important in the spread of urinary tract infections.
Below the openings of the ejaculatory ducts the epithelium changes to a pseudostratified or stratified columnar type, which lines the membranous urethra and the major part of the penile urethra Mucus-secreting cells are common throughout this epithelium and frequently occur in small clusters in the penile urethra. Branching tubular paraurethral glands secrete protective mucus onto the urethral epithelial lining and are especially numerous on its dorsal aspect. In older men many of the deep recesses of the urethral mucosa contain concretions similar to those found within prostatic glands (p. 1302). Towards the distal end of the penile urethra the epithelium changes once again, becoming stratified squamous in type with well-defined connective tissue papillae. This epithelium also lines the navicular fossa and becomes keratinized at the external meatus. The epithelial cells lining the navicular fossa are glycogen-rich. This may provide a substrate for commensal lactobacilli which, as in the female vagina (p. 1353), provide a defence against pathogenic organisms.
ref:-gray anatomy

Which is not a feature of benign hypertension in Kidney-

a)Hyaline arteriosclerosis
b)Interstitial lobular fibrosis
c)Medial hypertrophy of small vessels
d)Fibrinoid necrosis

Ans. is ‘d’ i.e., Fibrinoid necrosis [Ref : Robbin’s 7Th/e p. 1006, 1007 & 6e p. [snip],[snip] p. [snip]

Whether it is “essential” or of known etiology, hypertension results in
development of intrinsic lesions of the renal arterioles (hyaline arteriolosclerosis)
that eventually lead to loss of function (nephrosclerosis)…
harrison 1813 17th ed

“Essential” Hypertension (Arteriolar Nephrosclerosis)(BENIGN):-The characteristic pathology is in the afferent arterioles, which have
thickened walls due to deposition of homogeneous eosinophilic material
(hyaline arteriolosclerosis). Narrowing of vascular lumina results,
with consequent ischemic injury to glomeruli and tubules.Two processes participate in inducing the arterial lesions:
Medial and intimal thickening, as a response to hemodynamic changes, genetic defects, or both
Hyaline deposition in arterioles, caused partly by extravasation of plasma proteins through injured endothelium and partly by increased deposition of basement membrane matrix

Malignant nephrosclerosis is the form of renal disease associated with the malignant or accelerated phase of hypertension.The basis for this turn for the worse in hypertensive subjects is unclear, but the following sequence of events is suggested. The initial event appears to be some form of vascular damage to the kidneys. This most commonly results from long-standing benign hypertension, with eventual injury to the arteriolar walls, or it may spring from arteritis or a coagulopathy. In either case, the result is increased permeability of the small vessels to fibrinogen and other plasma proteins, endothelial injury, and platelet deposition. This leads to the appearance of fibrinoid necrosis


Linear deposition of lgG on glomerular basementmembrane is seen in —
b)Good pasteur’s syndrome
c)Nephrotic syndrome
d)Shunt nephritis

Ans. is ‘b’ i.e., Good pasture’s syndrome [Ref; Robbin’s 7E p. 976, 977 & 6E p. 951]

Patients who develop autoantibodies directed against glomerular
basement antigens frequently develop a glomerulonephritis termed
antiglomerular basement membrane (anti-GBM) disease. When they
present with lung hemorrhage and glomerulonephritis, they have a
pulmonary-renal syndrome called Goodpasture’s syndrome. The target epitopes for this autoimmune disease lie in the quaternary structure of α3 NC1 domain of collagen IV.

The presence of anti-GBM antibodies
and complement is recognized on biopsy by linear immunofluorescent
staining for IgG (rarely IgA).

Prognosis at presentation is worse if there are >50% crescents on renal
biopsy with advanced fibrosis, if serum creatinine is >5–6 mg/dL, if oliguria is present, or if there is a need for acute dialysis. Although frequently attempted, most of these latter patients will not respond to
plasmapheresis and steroids. Patients with advanced renal failure who
present with hemoptysis should still be treated for their lung hemorrhage,
as it responds to plasmapheresis and can be lifesaving. Treated
patients with less severe disease typically respond to 8–10 treatments
of plasmapheresis accompanied by oral prednisone and cyclophosphamide
in the first 2 weeks.

The worst prognosis for renal cell carcinoma is-

a)Vascular invasion
b)Associated with hyper calcemia
c)Presence of Hematuria
d)Size more than 5 cm.

Ans. is ‘a’ i.e., Vascular invasion [Ref : Robbin’7E. 1018 & 6E p. 993,]

Two staging systems used are the Robson classification and the American
Joint Committee on Cancer (AJCC) staging system. According to
the AJCC system, stage I tumors are <7 cm in greatest diameter and confined to the kidney, stage II tumors are ≥7 cm and confined to the
kidney, stage III tumors extend through the renal capsule but are confined to Gerota’s fascia (IIIa) or involve a single hilar lymph node
(N1), and stage IV disease includes tumors that have invaded adjacent
organs (excluding the adrenal gland) or involve multiple lymph
nodes or distant metastases
. The rate of 5-year survival varies by
stage: >90% for stage I, 85% for stage II, 60% for stage III, and 10%
for stage IV. HARRISON 593 17TH ED

Two staging systems used commonly are the Robson classification and the American Joint Committee on Cancer (AJCC) staging system. According to the former, stage I tumors are confined to the kidney; stage II tumors extend through the renal capsule but are confined to Gerota’s fascia; stage III tumors involve the renal vein or vena cava (stage III A) or the hilar lymph nodes (stage III B); and stage IV disease includes tumors that are locally invasive to adjacent organs (excluding the adrenal gland) or distant metastases. Five-year survival rate varies by stage: 66% for stage I, 64% for stage II, 42% for stage III, and 11% for stage IV. The prognosis for patients with stage IIIA lesions is similar to that of stage II disease, whereas the 5-year survival rate for patients with stage IIIB lesions is only 20%, closer to that of stage IV.
Harrison 15th ed p 607 describes Robson Classification

Minimal-change nephropathy—
a)Is the commonest cause of the nephrotic syndrome in childhood
b)Does not relapse after remission
c)Produces highly selective proteinuria
d)Does not cause depression of the serumcomplement level
e)Must always be confirmed by renal biopsy

Ans. Three options are correct i.e., a, c & d [Ref : Robbin’s 7th/e p. [snip], [snip] & 6th/e p. 954 & 956,]

MCD, sometimes known as nil lesion, causes 70–90% of nephrotic
syndrome in childhood
but only 10–15% of nephrotic syndrome in
adults.harrison 17th ed 1790

In children, the abnormal urine principally
contains albumin with minimal amounts of higher molecular weight
proteins, and is sometimes called selective proteinuria.

Relapses occur in 70–75% of children after the first remission, and
early relapse predicts multiple subsequent relapses.

Renal biopsy is a valuable tool in adults with nephrotic syndrome for establishing a definitive diagnosis, guiding therapy, and estimating prognosis. Renal biopsy is not required in the majority of children with nephrotic syndrome as most cases are due to MCD and respond to empiric treatment with glucocorticoids. harrison 15th ed 1585

Splliting of the glomerular basement membraneis seen in —
a)Acute glomerulonephritis
b)Membranous glomerulonephritis
c)Membranoproliferative glomerulonephritis
d)Good pasture’s syndrome

Ans. is ‘c’ i.e., Membranoproliferative glomerulonephritis [Ref : Robbin’s 7e p [snip] & 6e p. 959]

The glomeruli have a “lobular” appearance accentuated by the proliferating mesangial cells and increased mesangial matrix (Fig. 21-23) . The GBM is clearly thickened, often focally, most evident in the peripheral capillary loops. The glomerular capillary wall often shows a “double-contour” or “tram-track” appearance, especially evident in silver or PAS stains. This is caused by “duplication” of the basement membrane and the inclusion within the lamina rara interna of processes of cells extending into the peripheral capillary loops, so-called mesangial and monocyte interposition.

Type I MPGN, the most proliferative of the three types, shows mesangial
proliferation with lobular segmentation on renal biopsy and mesangial interposition between the capillary basement membrane
and endothelial cells, producing a double contour sometimes called
(Figs. e9-7 and e9-9). Subendothelial deposits with low
serum levels of C3 are typical, although 50% of patients have normal
levels of C3 and occasional intra-mesangial deposits.

Low serum C3 and a dense thickening of the GBM containing ribbons of dense deposits
and C3 characterize Type II MPGN, sometimes called dense deposit
disease (Fig. e9-8). Classically, the glomerular tuft has a lobular
appearance; intramesangial deposits are rarely present and subendothelial deposits are generally absent.

Proliferation in Type III MPGN is less common than the other two types and is often focal; mesangial interposition is rare, and subepithelial deposits can occur along widened segments of the GBM that appear laminated and disrupted.

The intracytoplasmic vacuoles seen in the Armmani Epstein cell are rich in –
a) Na and K’
b) Glycogen
c) Lipids
d) None of the above

ans is B

Glycogen vacuolation of the terminal part of the proxcimal convoluted tubules (loops of Henle) in diabetic patients, directly related to hyperglycemia and glycosuria..Ref INTERNET

Findings of multiple myeloma in kidney are –

a)Tubular casts
c)Wire loop lesions
d)Renal tubular necrosis

Ans. Four options are correct i.e., a, b, d & e [Ref : Robbin’s 7’/e p. 1005, 1006 & 6THe p. [snip] & [snip];Harrison 16th/e p. 1647 & 13Th/e p. 1544 for V]


Multiple Myeloma
Nonrenal malignant tumors, particularly those of hematopoietic origin, affect the kidneys in a number of ways (Table 21-11) . The most common involvements are tubulointerstitial, caused by complications of the tumor (hypercalcemia, hyperuricemia, obstruction of ureters) or therapy (irradiation, hyperuricemia, chemotherapy, infections in immunosuppressed patients). As the survival rate of patients with malignant neoplasms increases, so do these renal complications. We limit the discussion to the renal lesions in multiple myeloma that sometimes dominate the clinical picture in patients with this disease.
Renal involvement is a sometimes ominous manifestation of multiple myeloma; overt renal insufficiency occurs in half the patients with this disease. Several factors contribute to renal damage:
1.Bence Jones proteinuria and cast nephropathy. The main cause of renal dysfunction is related to Bence Jones (light-chain) proteinuria, because renal failure correlates well with the presence and amount of such proteinuria and is extremely rare in its absence. Two mechanisms appear to account for the renal toxicity of Bence Jones proteins. First, some light chains are directly toxic to epithelial cells; different light chains have different nephrotoxic potential. Second, Bence Jones proteins combine with the urinary glycoprotein (Tamm-Horsfall protein) under acidic conditions to form large, histologically distinct tubular casts that obstruct the tubular lumina and also induce a peritubular inflammatory reaction (cast nephropathy).

2.Amyloidosis, which occurs in 6% to 24% of patients with myeloma

3.Light-chain nephropathy. In some patients, light chains deposit in glomeruli in nonfibrillar forms, causing a glomerulopathy(described earlier), or around tubules, causing a tubulointerstitial nephritis.
Hypercalcemia and hyperuricemia, which are often present in these patients
4.Vascular disease in the usually elderly population affected with myeloma
5.Urinary tract obstruction with secondary pyelonephritis

Bilarerally symmmetrical contracted scarred kidney is seen in-
b)Chronic glomerulonephriris
c)End stage renal disease
d)Chronic pyelonephritis

Chronic obstructive pyelonephritis may be insidious in onset or may present the clinical manifestations of acute recurrent pyelonephritis with back pain, fever, frequent pyuria, and bacteriuria. Chronic pyelonephritis associated with reflux may have a silent onset. These patients come to medical attention relatively late in the course of their disease because of the gradual onset of renal insufficiency and hypertension or because of the discovery of pyuria or bacteriuria on routine examination. Reflux nephropathy is a common cause of hypertension in children. Loss of tubular function–in particular of concentrating ability–gives rise to polyuria and nocturia. Radiographic studies show asymmetrically contracted kidneys with characteristic coarse scars and blunting and deformity of the calyceal system.

Chronic Glomerulonephritis-The kidneys are symmetrically contracted and have diffusely granular, cortical surfaces. On section, the cortex is thinned, and there is an increase in peripelvic fat.

Cylindrical dilatation of renal tubules is seen in –
a)Polycystic disease ‘of kidney(Jipmer 95)
b)Medullary cystic disease
c)Wilms tumour
d)Lipoid nephrosis

Ans. is ‘a’ i.e., Polycystic disease of kidney [Ref : Robbin’s 7h/e p. 966 & 6ep. 940, see morphology 9th line]

This rare developmental anomaly is genetically distinct from adult polycystic kidney disease, having an autosomal recessive type of inheritance. Perinatal, neonatal, infantile, and juvenile subcategories have been defined, depending on time of presentation and presence of associated hepatic lesions. The first two are most common; serious manifestations are usually present at birth, and the young infant may succumb rapidly to renal failure.
Kidneys are enlarged and have a smooth external appearance. On cut section, numerous small cysts in the cortex and medulla give the kidney a spongelike appearance. Dilated elongated channels are present at right angles to the cortical surface, completely replacing the medulla and cortex (Fig. 21-8 C). On microscopic examination, there is saccular or, more commonly, cylindrical dilation of all collecting tubules. The cysts have a uniform lining of cuboidal cells, reflecting their origin from the collecting tubules. The disease is invariably bilateral. In almost all cases, there are multiple epithelium-lined cysts in the liver (Fig. 21-8 D) as well as proliferation of portal bile ducts.
Patients who survive infancy (infantile and juvenile form) may develop a peculiar type of hepatic fibrosis characterized by bland periportal fibrosis and proliferation of well-differentiated biliary ductules, a condition now termed congenital hepatic fibrosis. In older children, the hepatic picture in fact predominates. Such patients may develop portal hypertension with splenomegaly. Curiously, congenital hepatic fibrosis sometimes occurs in the absence of polycystic kidneys and has been reported occasionally in the presence of adult polycystic kidney disease.

FOR THE ABOVE QUESTION:-At birth the kidneys are enlarged with a smooth external surface. The distal tubules and collecting ducts are dilated into elongated cysts that are arranged in a radial fashion. As the patient ages, the cysts may become more spherical and the disease can be confused withADPKD. Interstitial fibrosis is also seen as renal function deteriorates. Liver involvement includes proliferation and dilation of small intrahepatic bile ducts as well as periportal fibrosis.


Flea bitten kidney is seen in all of following except –

a)Malignant hypertension
c)Infective endocarditis

Malignant Nephrosclerosis and Accelerated Hypertension:
On gross inspection, the kidney size is dependent on the duration and severity of the hypertensive disease. Small, pinpoint petechial hemorrhages may appear on the cortical surface from rupture of arterioles or glomerular capillaries, giving the kidney a peculiar “flea-bitten” appearance.

HUS and TTP, consumptive coagulopathies characterized by microangiopathic hemolytic anemia and thrombocytopenia, have a particular predilection for the kidney and the central nervous system, the latter especially in TTP. The kidneys of patients with HUS or TTP often exhibit a “flea-bitten” appearance, the result of multiple cortical hemorrhagic infarcts.HARRISON 15TH ED

Grossly, the kidneys in subacute bacterial endocarditis
have subcapsular hemorrhages with a “flea-bitten” appearance,
and microscopy on renal biopsy reveals a focal proliferation
around foci of necrosis associated with abundant mesangial, subendothelial,
and subepithelial immune deposits of IgG, IgM, and C3.HARR 17TH ED 1787

The pathology in the kidney in classic PAN is that of arteritis
without glomerulonephritis. In patients with significant hypertension,
typical pathologic features of glomerulosclerosis may be seen. In addition,
pathologic sequelae of hypertension may be found elsewhere in
the body.

The protein in glomerular basement membraneresponsible for charge dependent filtration is –

b)Collagen type IV

Ans. is ‘c’ i.e., Proteoglycan

Figure 21-4 ROBBINS 6TH ED P 934 :-A proposed model of the GBM molecular architecture in which type IV collagen monomers (gray) form a stable network through their NC1 domains (dimeric interactions, gray spheres) and 7S domains (tetrameric interactions) and intertwine along the triple-helical domains. Laminin monomers (red) separately form a reversible meshwork. Entactin (green) connects laminin to the collagen network and binds to perlecan (blue), an anionic heparan sulfate proteoglycan. This anionic suprastructure determines the charged porous nature of the GBM.
The major characteristics of glomerular filtration are an extraordinary high permeability to water and small solutes, accounted for by the highly fenestrated endothelium, and impermeability to proteins, such that molecules of the size of albumin (+3.6-nm radius; 70,000 MW). The latter property, called glomerular barrier function, discriminates among various protein molecules, depending on their size (the larger, the less permeable) and charge (the more cationic, the more permeable). This size- and charge-dependent barrier function is accounted for by the complex structure of the capillary wall, the collagenous porous charged suprastructure of the GBM, and the many anionic moieties present within the wall, including the acidic proteoglycans of the GBM (Fig. 21-4) and the sialoglycoproteins of epithelial and endothelial cell coats. The charge-dependent restriction is important in the virtually complete exclusion of albumin from the filtrate, because albumin is an anionic molecule of a pI 4.5. The visceral epithelial cell is important in the maintenance of glomerular barrier function: its slit diaphragm presents a distal diffusion barrier to the filtration of proteins, and it is the cell type that is largely responsible for synthesis of GBM components

Lipid cast are seen in –
a)Acute tubular necrosis
b)Nephrotic syndrome
c)Cytomegalic inclusion disease

Ans. is ‘b’ i.e., Nephrotic syndrome [Ref : Robbin’s 7e p. 979 & 6E p. 953]
Due to increased lipoproteins, lipoproteins leak across the glomerular capilary wall and the lipids appear in the urine either as free fat or as oval fat bodies representing lipoproteins absorbed by tubular epithelial cellsand then shed along with degenerated cells.

Benign hypertension is associated with –
a) Hyline arteriosclerosis
b) Fibrinoid necrosis
c) Basal ganglia
d) Periventricle

Ans. is ‘a’ i.e., Hyaline arteriosclerosis [Ref : Robbin’s 7″/e p. 1006 & 6fhle p. [snip]]

A patient presenting with haemoptysis and renal failure with anti basement membrane antibodies has –
a) Good pasture’s
b) Wegener’s
c) Churg Strauss
d) Henoch-scholein purpura

Ans. is ‘a’ i.e., Good pasture’s syndrome [Ref : Robbin’s 7/e p. 976 & 6/e p. 951]

Bilateral contracted granular kidney seen in all except-
a)Chronic Pyelonephritis
b)Chronic glomerulonephritis
c)Benign Nephrosclerosis
d)Diabetic nephropathy

Ans. is `d’ i.e., Diabetic nephropathy [Ref : Chandrasoma taylor 3”/e p. 725, table (49.2)]

already discussed

Crescents in post-streptococal glomerulonephritis are –
a)Epithelial cells
b)Mesangial cells
c)Epithelial, mesangial & macrophages
d)Macrophages only

Ans. is a and b

harrison—A crescent is a half-moon-shaped collection of cells in Bowman’s space, usually composed of proliferating parietal epithelial cells and infiltrating monocytes.The classic pathologic correlate of RPGN is crescent formation involving most glomeruli (crescentic glomerulonephritis), crescents being half-moon-shaped lesions in Bowman’s space composed of proliferating parietal epithelial cells and infiltrating monocytes (extracapillary proliferation).

robbins—Crescents are formed by proliferation of parietal cells and by migration of monocytes and macrophages into Bowman space. Neutrophils and lymphocytes may be present. The crescents eventually obliterate Bowman space and compress the glomerular tuft.

Thickening of basement membrane of glomeruliis seen in –
a)IgA nephropathy
b)Membranoproliferative glomerulonephritis
c)Lipoid nephrosis
d)Post streptococcal glomerulonephrities

Ans. is ‘b’ i.e., Membranoproliferative glomerulonephritis [Ref : Robbin’s 7e p. [snip] ]

Maximum endocapillary proliferation is seen in-
a)Membranous glomerulonephritis
b)Masangioproliferative glomerulonephritis
c)Focal segmental glomerulonephritis
d)Post streptococcal glomerulonephritis

ans is D


To illustrate the importance of the speed of onset, extent, and intensity of glomerular injury, it is instructive to compare two forms of immune complex glomerulonephritis, namely, acute postinfectious glomerulonephritis and IgA nephropathy. Postinfectious glomerulonephritis is characterized by rapid and extensive formation of immune complexes throughout the glomerular capillary wall, which often provokes acute renal failure with the classic hallmarks of acute inflammation: complement activation, leukocyte recruitment, lysosomal enzyme release, free radical generation, and perturbation of vascular tone and permeability. In contrast, IgA nephropathy is characterized by slow, but sustained, formation of immune complexes, largely confined to the mesangium; less dramatic activation of complement and other secondary mediator systems; and either stability ofGFR or progressive renal insufficiency over 10 to 20 years

Interstitial nephritis is caused by –
a) Methicillin
b) Ampicillin
c) Cloxacillin
d) Pencicillin


ref. Katzung Pharmacology p. 377

SIDE EFFECTS OF PENICILLIN:-Allergy: Allergic reactions include urticaria, severe pruritus, fever, joint swelling. hemolytic anemia, nephritis, and anaphylaxis. About 5-10% of persons with a past history
of penicillin reaction have an allergic response when given a penicillin again. Methicillin causes nephritis more often than do other penicillins, and nafcillin is associated with neutropenia. Antigenic determinants include degradation products of penicillins such as penicilloic acid. Complete cross-allergenicity between different penicillins should be as-
sumed. Ampicillin frequently causes maculopapular skin rash that may not be an allergic reaction.

Interstitial nephritis
A. Allergic: antibiotics (β-lactams, sulfonamides, quinolones, rifampin),
nonsteroidal anti-inflammatory drugs, diuretics, other drugs
B. Infection: pyelonephritis (if bilateral)
C. Infiltration: lymphoma, leukemia, sarcoidosis
D. Inflammatory, nonvascular: Sjögren’s syndrome, tubulointerstitial
nephritis with uveitis

Harrison 17th ed 1753

Virtually any pharmacologic agent may
trigger allergic interstitial nephritis, which is characterized by infiltration
of the tubulointerstitium by granulocytes (typically but not invariably
eosinophils), macrophages, and/or lymphocytes and by
interstitial edema. The most common offenders are antibiotics (e.g.,
penicillins, cephalosporins, quinolones, sulfonamides, rifampin) and

Fever, arthralgias, and a pruritic erythematous
rash following exposure to a new drug suggest allergic interstitial nephritis,
although systemic features of hypersensitivity are frequently

(See also Chap. e9) Anuria suggests complete urinary tract obstruction
but may complicate severe cases of prerenal or intrinsic renal ARF.
Wide fluctuations in urine output raise the possibility of intermittent
obstruction, whereas patients with partial urinary tract obstruction
may present with polyuria due to impairment of urine concentrating
In prerenal ARF, the sediment is characteristically acellular and
contains transparent hyaline casts (“bland,” “benign,” “inactive” urine
sediment). Hyaline casts are formed in concentrated urine from normal
constituents of urine—principally Tamm-Horsfall protein, which
is secreted by epithelial cells of the loop of Henle. Postrenal ARF may
also present with an inactive sediment, although hematuria and pyuria
are common in patients with intraluminal obstruction or prostatic
disease. Pigmented “muddy brown” granular casts and casts containing
tubule epithelial cells are characteristic of ATN and suggest an ischemic
or nephrotoxic etiology. These casts are usually found in
association with mild “tubular” proteinuria (<1 g/d), reflecting impaired
reabsorption and processing of filtered proteins by injured
proximal tubules. Casts may be absent in 20–30% of patients with
ATN and are not required for diagnosis. In general, red blood cell casts
indicate glomerular injury or, less often, acute tubulointerstitial nephritis.
White cell casts and nonpigmented granular casts suggest interstitial
, whereas broad granular casts are characteristic of
chronic kidney disease and probably reflect interstitial fibrosis and
dilatation of tubules. Eosinophiluria (>5% of urine leukocytes) is a
common finding (~90%) in antibiotic-induced allergic interstitial nephritis
and can be detected with Hansel’s stain; however, lymphocytes
may predominate in allergic interstitial nephritis induced by NSAIDs
and some other drugs (i.e., ampicillin, rifampicin, and interferon α).
Occasional uric acid crystals (pleomorphic in shape) are common in
the concentrated urine of prerenal ARF but suggest acute urate nephropathy
if seen in abundance. Oxalate (envelope-shaped) and hippurate
(needle-shaped) crystals raise the possibility of ethylene glycol
ingestion and toxicity.

Acute Drug-Induced Interstitial Nephritis
This is a well-recognized adverse reaction to a constantly increasing number of drugs. First reported after the use of sulfonamides, acute tubulointerstitial nephritis most frequently occurs with synthetic penicillins (methicillin, ampicillin), other synthetic antibiotics (rifampin), diuretics (thiazides), NSAIDs (phenylbutazone), and miscellaneous drugs (phenindione, cimetidine)

Tamm-Horsefall protein is produced in-
a) Kideny
b) Liver
c) Plasma cells
d) None
Ans. is ‘a’ i.e., Kidney [Ref : Robbin’s 7h/e p. 995 & 6′”/e p. 970]

Eosinophilic hyaline casts, as well as pigmented granular casts, are common, particularly in distal tubules and collecting ducts. These casts consist principally of Tamm-Horsfall protein (a specific urinary glycoprotein normally secreted by the cells of ascending thick limb and distal tubules) in conjunction with hemoglobin, myoglobin, and other plasma proteins.

Histopathology showing large cells with plant like apperance with perinuclear halo is seen in
which type of renal cell carcinoma ?-(PGI 2K)
a) Onchocytoma
b) Granular cell carcinoma
c) Angiosarcoma
d) Chromophobic
e)Clear cell carcinoma

Ans. is ‘d’ i.e., Chromophobic [Ref : Robbin’s 7e p. 1018 & 6e p. 993]

Sub-epithelial humps are characteristic of –
a)Minimal change glomerulonephritis
b)Membranous glomerulonephritis
c)Membranoproliferative glomerulonephritis
d)Post-steptococcal glomerulonephritis

Ans. is ‘d’ i.e., Post-streptococcal glomerulonephritis [Ref : Robbin’s 7e p. 975 & 6e p. 950]

The renal biopsy in poststreptococcal glomerulonephritis demonstrates
hypercellularity of mesangial and endothelial cells, glomerular
infiltrates of polymorphonuclear leukocytes, granular subendothelial
immune deposits of IgG, IgM, C3, C4, and C5-9, and subepithelial deposits
(which appear as “humps”) (Fig. e9-4).harrison 17 e

Onion skin lesions, in the muscular layer ofarteriole, are seen in
b)Benign nephrosclerosis
c)Malignant nephrosclerosis
d). RPGN

“Malignant” Hypertension–The kidneys are characterized
by a flea-bitten appearance resulting from hemorrhages in
surface capillaries. Histologically, two distinct vascular lesions can be
seen. The first, affecting arterioles, is fibrinoid necrosis, i.e., infiltration of arteriolar walls with eosinophilic material including fibrin, thickening of vessel walls, and, occasionally, an inflammatory infiltrate (necrotizing arteriolitis). The second lesion, involving the interlobular
arteries, is a concentric hyperplastic proliferation of the cellular elements
of the vascular wall with deposition of collagen to form a hyperplastic
arteriolitis (onion-skin lesion).

Ewing sarcoma usually arises in the diaphysis of long tubular bones, especially the femur and the flat bones of the pelvis. It presents as a painful enlarging mass, and the affected site is frequently tender, warm, and swollen. Some patients have systemic findings, including fever, elevated sedimentation rate, anemia, and leukocytosis, which mimic infection. Plain x-rays show a destructive lytic tumor that has permeative margins. The characteristic periosteal reaction produces layers of reactive bone deposited in an onion-skin fashion.

In its macroscopic appearance, the renal cell carcinoma tumor is characteristic. It may arise in any portion of the kidney, but more commonly it affects the poles, particularly the upper one. Clear cell neoplasms occur as solitary unilateral lesions. They are spherical masses, 3 to 15 cm in diameter, composed of bright yellow-gray-white tissue that distorts the renal outline. There are commonly large areas of ischemic, opaque, gray-white necrosis, foci of hemorrhagic discoloration, and areas of softening. The margins are usually sharply defined and confined within the renal capsule (Fig. 21-59) . Papillary tumors can be multifocal and bilateral. They are typically hemorrhagic and cystic, especially when large. The papillae may be seen grossly as golden yellow flakes.
As tumors enlarge, they may bulge into the calyces and pelvis and eventually may fungate through the walls of the collecting system to extend even into the ureter. One of the striking characteristics of this tumor is its tendency to invade the renal vein (Fig. 21-59) and grow as a solid column of cells within this vessel. Further extension produces a continuous cord of tumor in the inferior vena cava and even in the right side of the heart.
In clear cell carcinoma, the growth pattern varies from solid to trabecular (cordlike) or tubular (resembling tubules). The tumor cells have a rounded or polygonal shape and abundant clear or granular cytoplasm; the latter on special stains contains glycogen and lipids (Fig. 21-60 A). The
tumors have delicate branching vasculature and may exhibit cystic as well as solid areas. Most tumors are well differentiated, but some show marked nuclear atypia with formation of bizarre nuclei and giant cells. Papillary carcinoma is composed of cuboidal or low columnar cells arranged in papillary formations. Interstitial foam cells are common in the papillary cores (Fig. 21-60 B). Psammoma bodies may be present. The stroma is usually scanty but highly vascularized. Chromophobe renal carcinoma is made up of pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a concentration of the largest cells around blood vessels (Fig. 21-60 C). Collecting duct carcinoma is a rare variant showing irregular channels lined by highly atypical epithelium with a hobnail pattern. Sarcomatoid changes arise infrequently in all types of renal cell carcinoma and are a decidedly ominous feature of these tumors.

Membranous glomerulopathy. Membranous glomerulopathy
is due to subepithelial deposits, with resulting basement membrane
reaction, resulting in the appearance of spike-like projections on
silver stain.

Poststreptococcal glomerulonephritis, lupus nephritis,
and idiopathic membranous nephritis typically are associated with immune
deposits along the GBM, while anti-GBM antibodies are produced
in anti-GBM disease. Preformed circulating immune complexes
can precipitate along the subendothelial side of the GBM, while other
immune deposits form in situ on the subepithelial side. These latter
deposits accumulate when circulating autoantibodies find their antigen
trapped along the subepithelial edge of the GBM.

Immunofluorescent and electron microscopy can detect
the presence and location of subepithelial, subendothelial, or mesangial
immune deposits, or reduplication or splitting of the basement membrane.

Membranous glomerulopathy. Membranous glomerulopathy
is due to subepithelial deposits, with resulting basement membrane
reaction, resulting in the appearance of spike-like projections on
silver stain (left). The deposits are directly visualized by fluorescent anti-
IgG, revealing diffuse granular capillary loop staining (middle). By electron microscopy, the subepithelial location of the deposits and early surrounding basement membrane reaction is evident, with overlying foot
process effacement (right). (ABF/Vanderbilt Collection.)

Postinfectious (poststreptococcal) glomerulonephritis.
The glomerular tuft shows proliferative changes with numerous
PMNs, with a crescentic reaction in severe cases (left). These
deposits localize in the mesangium and along the capillary wall in a
subepithelial pattern and stain dominantly for C3 and to a lesser extent
for IgG (middle). Subepithelial hump-shaped deposits are seen
by electron microscopy (right). (ABF/Vanderbilt Collection.)

Subendothelial deposits not seen in membranous nephritis type while spike pattern is seen there.In poststreptococcal subendothelial and subepithelial deposits are seen but there is hump of subepithelial deposits instead.
Uremia occurs when total GFR is reduced by
a) 25% b) 50%
c) 60% d) 80%

Ans. is ‘a’ i.e., 25% [Ref : Patho. Robbins 7Th/e p. 961 & 6′”/e p. 936]

It should be emphasized that the signs and symptoms of uremia
will develop at significantly different levels of serum creatinine depending
upon the patient (size, age, and sex), the underlying renal disease,
existence of concurrent diseases, and true GFR. In general, patients do not develop symptomatic uremia until renal insufficiency is usually quite severe (GFR < 15 mL/min).HARRISON 17TH ED 269

Uremia. The red cells in uremia may acquire numerous,
regularly spaced, small spiny projections. Such cells, called burr cells or echinocytes, are readily distinguishable from irregularly spiculated

Acanthocytosis. Spiculated red cells are of two types:
acanthocytes are contracted dense cells with irregular membrane projections that vary in length and width; echinocytes
have small, uniform, and evenly spaced membrane projections. Acanthocytes are present in severe liver disease, in patients with abetalipoproteinemia, and in rare patients with McLeod blood group. Echinocytes are found in patients with severe uremia, in glycolytic red cell enzyme defects, and in microangiopathic hemolytic anemia.

Clinical feature of CRF appear when renal function is reduce to
a) 70% b) 50%
c) 30% d) 20% of normal

Ans. is ‘d’ i.e., 20% of normal [Ref : Patho. Robbins 7e p. 961 & 6e p. 936]

Acute renal failure is dominated by oliguria or anuria (no urine flow), with recent onset of azotemia. It can result from glomerular (e.g., crescentic glomerulonephritis), interstitial, and vascular injury or acute tubular necrosis.

Chronic renal failure, characterized by prolonged symptoms and signs of uremia, is the end result of all chronic renal diseases.

Uremia or uraemia is a term used to loosely describe the illness accompanying kidney failure (also called renal failure), in particular the nitrogenous waste products associated with the failure of this organ.

Azotemia is another word that refers to high levels of urea, but is used primarily when the abnormality can be measured chemically but is not yet so severe as to produce symptoms. Uremia can also result in fibrinous pericarditis.

All of the following may be associated with massive proteinuria except –
b)Renal vein thrombosis
c)Polycystic kidneys
d)Polyarteritis nodosa

ans is C and D

Renal artery thrombosis may lead to mild proteinuria and hematuria, whereas renal vein thrombosis typically induces heavy proteinuria and hematuria.

Amyloidosis also ass with heavy protenuria
Polycystic Kidney ass with mild proteinuria.
PAN is also ass with mild proteinuria as it produces nephritic syndrome.
Harrison 1785 17th ed

CLINICAL SYNDROMES Various forms of glomerular injury can also be parsed into several distinct syndromes on clinical grounds (Table 277-2). These syndromes, however, are not always mutually exclusive.There is an acute nephritic syndrome producing 1–2 g/24 h ofproteinuria,hematuria
with red blood cell casts, pyuria,
hypertension, fluid retention, and a rise in serum creatinine associated with a reduction
in glomerular filtration. If glomerular inflammation develops slowly, the serum creatinine will rise gradually over many weeks, but if the serum creatinine rises quickly, particularly over a few days, acute
nephritis is sometimes called rapidly progressive glomerulonephritis (RPGN); the histopathologic term crescentic glomerulonephritis
refers to the clinical occurrence of RPGN in a patient with this characteristic glomerular lesion. When patients with RPGN present with lung hemorrhage from Goodpasture’s syndrome, antineutrophil cytoplasmic antibodies (ANCA) small-vessel vasculitis, lupus erythematosus, or cryoglobulinemia, they are often diagnosed as
having a pulmonary-renal syndrome. Nephrotic syndrome describes the onset of heavy proteinuria (>3.0 g/24 h), hypertension,hypercholesterolemia, hypoalbuminemia, edema/anasarca, and microscopic hematuria;if only large amounts of proteinuria
are present without clinical manifestations, the condition is sometimes called nephrotic-range proteinuria. The glomerular filtration
rate (GFR) in these patients may initially be normal or, rarely, higher than
normal, but with persistent hyperfiltration and continued nephron loss, it typically declines over months to years. Patients
with a basement membrane syndrome either have genetically abnormal basement membranes or an autoimmune response to
basement membrane collagen IV associated with microscopic hematuria, mild to heavy proteinuria, and hypertension with variable elevations in serum creatinine. Glomerular-vascular syndrome describes patients
with vascular injury producing hematuria and moderate proteinuria. Affected individuals can have vasculitis, thrombotic microangiopathy, antiphospholipid syndrome, or, more commonly, a systemic disease
such as atherosclerosis, cholesterol emboli, hypertension, sickle cell anemia, and autoimmunity. Infectious diseases-asso-ciated syndrome is most important if one has an international perspective.Save for subacute bacterial endocarditis in the Western Hemisphere, malaria and schistosomiasis may be the most commoncauses of glomerulonephritis throughout the world, closelyfollowed by HIV and chronic hepatitis B and C. These infectiousdiseases produce a variety of inflammatory reactions in glomerular capillaries, ranging from nephrotic syndrome to acute nephritic injury,and yield urinalyses that demonstrate a combination of hematuria and proteinuria.

Wilm’s tumour may be associated with all except –
a)Genitourinary anomalies
b)Beckwith’s syndrome

Ans. is ‘d’ i.e., Glaucoma [Ref Patho Robins 7e p. 504, 505 & 6e p. 488 ]

Wilms’ tumor is the most common primary renal tumor of childhood, usually diagnosed between the ages of 2 and 5 years.

Neuroblastoma is one of the most common childhood solid tumors and is the most common tumor diagnosed in infants less than 1 year of age

Neoplasms that exhibit sharp peaks in incidence in children younger than 10 years of age include (1) leukemia (principally acute lymphoblastic leukemia); (2) neuroblastoma; (3) Wilms’ tumor; (4) hepatoblastoma; (5) retinoblastoma; (6) rhabdomyosarcoma; (7) teratoma; (8) Ewing sarcoma; and, finally, posterior fossa neoplasms–principally (9) juvenile astrocytoma, (10) medulloblastoma, and (11) ependymoma

Hemangiomas: (benign) are the most common tumors of infancy.

The risk of Wilms’ tumor is increased in association with at least three recognizable groups of congenital malformations exhibiting aberrations in at least two distinct chromosomal loci.
1.The first group of patients have the WAGR syndrome characterized by aniridia, genital anomalies, and mental retardation and have a 33% chance of developing Wilms’ tumor.
2.A second group of patients at risk for Wilms’ tumor have the Denys-Drash syndrome, which is characterized by gonadal dysgenesis (male pseudohermaphroditism) and nephropathy leading to renal failure. The majority of these patients develop Wilms’ tumors.
3.Clinically distinct from these previous two groups of patients but also having an increased risk of developing Wilms’ tumor are those children with Beckwith-Wiedemann syndrome, characterized by enlargement of body organs, hemihypertrophy, renal medullary cysts, and abnormal large cells in adrenal cortex (adrenal cytomegaly).

Which one the following variants of renal cell carcinoma has the worst prognosis –
)a) Papillary b) Tubuloalveolar
c) Chromophobe d) Sacromatoid

no idea

Renal cell neoplasia represents a heterogeneous group of tumors with
distinct histopathologic, genetic, and clinical features ranging from
benign to high-grade malignant (Table 90-3). They are classified on
the basis of morphology and histology. Categories include clear cell
carcinoma (60% of cases), papillary tumors (5–15%), chromophobic
tumors (5–10%), oncocytomas (5–10%), and collecting or Bellini
duct tumors (<1%). Papillary tumors tend to be bilateral and multifocal.
Chromophobic tumors have a more indolent clinical course, and
oncocytomas are considered benign neoplasms. In contrast, Bellini
duct carcinomas, which are thought to arise from the collecting ducts
within the renal medulla, are very rare but very aggressive. They tend
to affect younger patients.

The renal tumour which has multicentric origin –a)Wilm’s tumour(TN [snip])
b)Transitional cell carcinoma
c)Squamous cell carcinoma
d)Renal cell carcinoma


Related to the molecular genetic and corresponding heterogeneity of Wilms’ tumor is the recognition of a premalignant or precursor lesion in many of these cases– nephroblastomatosis. This term refers to multicentric or diffuse foci of immature nephrogenic elements within areas of otherwise non-neoplastic kidney parenchyma. [86] Recognition of this lesion is important because its presence implies a substantially increased risk of developing a Wilms’ tumor.
MORPHOLOGY.–Grossly, Wilms’ tumor tends to present as a large, solitary, well-circumscribed mass, although 10% are either bilateral or multicentric at the time of diagnosis. On cut section, the tumor is soft, homogeneous, and tan to gray with occasional foci of hemorrhage, cyst formation, and necrosis

In an adult Unilateral smooth contracted kidney with hypertension is seen in.-
a) Stenosis of renal artery
b) Chr. GN
c) Renal cell CA
d) Pyelonephritis

Ans. is ‘a’ i.e., Stenosis of renal artery [ Ref : Robbin’s Illustrated r/e p. 1009 & 63/4 p. [snip], 976]

The ischemic kidney is usually reduced in size and shows signs of diffuse ischemic atrophy, with crowded glomeruli, atrophic tubules, interstitial fibrosis, and focal inflammatory infiltrate. The arterioles in the ischemic kidney are usually protected from the effects of high pressure, thus showing only mild arteriolosclerosis, in contrast to the contralateral nonischemic kidney, which may exhibit hyaline arteriolosclerosis, depending on the severity of the preceding hypertension.

Crescents are derived from –
a)Epithelial cells + fibrin + macrophage
b)Mesangium + fibrin + macrophage
c)Tubule + mesangiaum + fibrin
d)Mesangiaum + fibrin

Ans. is ‘a’ i.e., Epithelium cells + fibrin + macrophage [Ref : Robbin’s Illustrated 7h/e p. 977 & 6e p.951]


Disease that recurs after transplantation of kidney is –
a) DM b) MPGN
c) SLE d) Mesangial

Ans. Two options are correct i.e., ‘a & b’ [Ref :Robbin’s Illustrated 7e p. 985, 984 & 6th/e p. 958, 959]”Diabetic lesions may recur in the renal allografts (r/e p. 992, 6e p. 968)”
“There is high incidence of recurrence in transplant patients in membranoproliferative glomerulonephritis,particularly in dense deposit disease”. —> (7″/e p. [snip], 6th/e p. 959)
“In focal segmental glomerulosderosis recurrences are seen in 25% to 50% of the patients receivingallograpts” r/e p. [snip], 6th/e p. 958

Disease that recurs after transplantation of kidney is –
a) DM b) MPGN
c) SLE d) Mesangial



While 1-year transplant survival is excellent, most recipients experience
progressive decline in kidney function over time thereafter. Chronic renal
transplant dysfunction can be caused by recurrent disease, hypertension,
cyclosporine or tacrolimus nephrotoxicity, chronic immunologic
rejection, secondary focal glomerulosclerosis, or a combination of these
. Chronic vascular changes with intimal proliferation
and medial hypertrophy are commonly found. Control of systemic and
intrarenal hypertension with ACE inhibitors is thought to have a beneficial
influence on the rate of progression of chronic renal transplant dysfunction.
Renal biopsy can distinguish subacute cellular rejection from
recurrent disease or secondary focal sclerosis.

All are true about minimal change GN except-

a)Selective proteinuria
b)IgG deposition in mesangium
c)Common in age group 2-9 years .
d)Responds to steroids

Ans. is ‘b’ i.e., IgG deposition in mesangium [ Ref : Robbin’s Illustrated 7h/e p. [snip]-[snip] & 6e p. 955]

In children, the abnormal urine principally contains albumin with minimal amounts of higher molecular weight proteins, and is sometimes called selective proteinuria.

Prednisone is first-line therapy, and other immunosuppressive
drugs, such as cyclophosphamide, chlorambucil, and mycophenolate
mofetil, are saved for frequent relapsers, steroid-dependent, or steroid resistant patients.

MCD, sometimes known as nil lesion, causes 70–90% of nephrotic
syndrome in childhood
but only 10–15% of nephrotic syndrome in
In reflux nephropathy, glomerular lesion is-
a) Focal G.N.
b) Membranous G.N.
c) Membrano proliferative G.N.
d) Minimal change disease

1014.Ans. is ‘a’ i.e., Focal G.N. [ Ref : Robbin’s Illustrated 7e p. 1000, 1001 & &6e p. 977]

1810 HARRISON 17TH ED…..Vesicoureteral Reflux (See also Chap. 283) When the function of the ureterovesical junction is impaired, urine may reflux into the ureters due to the high intravesical pressure that develops during voiding. Clinically, reflux is often detected on the voiding and postvoiding films obtained during intravenous pyelography, although voiding cystourethrography may be required for definitive diagnosis. Bladder infection may ascend the urinary tract to the kidneys through incompetent ureterovesical sphincters. Not surprisingly, therefore, reflux is often discovered in patients with acute and/or chronic urinary tract infections. With more severe degrees of reflux, characterized by dilatation of ureters and renal pelves, progressive renal damage often appears. Uncertainty exists as to the necessity of infection in producing the scarred kidney of reflux nephropathy.
Substantial proteinuria is often present, and glomerular lesions
similar to those of idiopathic focal glomerulosclerosis (Chap. 277)
are often found in addition to the changes of chronic tubulointerstitial
Surgical correction of reflux is usually necessary only with the
more severe degrees of reflux since renal damage correlates with the extent of reflux. Obviously, if extensive glomerulosclerosis already exists,
urologic repair may no longer be warranted
True about membranous GN are following except-
a)Thickening of B.M
b)Deposition between endothelium and B.M.
c)Most common cause of nephrotic syndrome in adults
d)Seen in SLE, tumors, drugs

Ans. is “b’ i.e., Deposition between endothelium and B.M. f Ref :Robbin’s illustrated 7Th/e p.[snip], [snip] & 6th/e p. 954]

Already discussed
In membranous glomerulopathy only subepithelial deposits seen.Not subendothelial.

Glomerulonephritis associated with AIDS is-

a) Focal segmental GN
d) Membranous GN

Ans. is ‘a’ i.e., Focal segmental GN [ Ref : Robbin’s Illustrated 7h/e p. [snip], [snip] & 6th/e p. 958,”Now collapsing glomerulopathy is the hall mark of AIDS”Harrison 15thle p. 1887]

Subepithelial deposits in kidney are seen in ALL EXCEPT-a)MPGN-1
b)GPS (good-pasture synd)
d)Membranous GN


There are no subepithelial deposits.

Crescents formed in bowmans space

Kidney disease with autosomal dominant inheritance
a) Juvenile nephrolithiasis
c) Medullary sponge kidney
d) Nephronopthisis

Ans. Two options are correct i.e., ‘b & c’ [ Ref : Robbin’s Illustrated 7h/e p. 962 & 6th/e p. 941]

Nephronophthisis (NPHP) is the most common genetic cause of ESRD in childhood and adolescence.Five distinct genetic mutations with autosomal recessive inheritance have been identified (Table 278-1 harrison 17th ed p.1799). Although their precise functions are unclear,
the defective protein products, named nephrocystins and inversin,
localize to the primary cilium and associated basal body of renal
epithelial cells, similar to the polycystins and fibrocystin.

10 Responses to “Kidney MCQs”

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