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Dr K Chaudhry
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by
Dr K Chaudhry
 
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Chapter 9
Urinary system
 
ACUTE GLOMERULONEPHRITIS

Etiology 

1. Secondary to infection in some site of the body; commonest cause is haemolytic strepto­coccal infection of the respiratory tract, other organisms may be pneumococcus, or Streptococcus viridans. 
2.  Nephritic symptoms appear 7-21 days after the onset of infection. 
3. May be associated with tonsillitis, dental sepsis, cervical adenitis, parotitis, subacute bacterial endocarditis, scarlet fever, measles, smallpox, diphtheria. 

Gross Appearance 
1. Kidney is enlarged, sometimes considerably 
2. Consistence reduced 
3. Capsule tense, strips with ease 
4. Outer surface smooth, pale grey or red, mottled 
5. Cuts with reduced resistance. 

Cut Surface 
1. Buldging, soft and moist. 
2. May bleed freely, depending upon the degree of accompanying hyperaemia. 
3. Cortex moderately or considerably thickened. 
4. Striations indistinct or broken. 
5. Glomeruli, appear as tiny white spots giving cortex a sanded appearance. 
6.  Pyramids may be slightly swollen, but are practically normal. 
7.  The peripelvic fat and pelvis normal. 

Microscopic Appearance 

Tubular Lesions 

1.  Retrogressive changes in tubular epithelium, affecting particularly that of proximal convoluted tubules. 
 (i) Cloudly swelling 
 (ii) Fatty degeneration 
 (iii) Hydropic degeneration 
 (iv) Hyaline degeneration 
 (v) Necrosis. 

2. Desquamative nephritis. Excessive desqua­mation of the degenerated and necrotic epithelium. 
3. Granular albuminous precipitate in the tubules and in the subcapsular space of glomerulus. 
4. Hyaline casts in the tubules; may show adherance of epithelium, leucocytes, or erythrocytes. 
5. Finely or coarsely granular epithelial, leuco­cytic, blood and fibrin casts may be observed. 
6. Hyperaemia and interstitial oedema. 
7. Occasionally, slight infiltration of lymphocytes and plasma cells. 

Glomerular Lesions 

Glomerular lesions may of three types. 

A. Acute degenerative glomerulitis 

1. Blood in the subcapsular space and adjacent tubules; resulting from deterioration of the cells of capillary loops. 
2.  Glomerular lesions not widespread. 

B. Acute exudative glomerulitis 
1. Non-suppurative lesion. 
2. Polymorphs present in the tuft, subcapsurar space and tubules. 
3. Rarely, tuft contains tiny abscesses.. 
4. Endothelial cells of capillaries swollen altering the glomerular function. 
5. Fibrin may be deposited in subcapsular space, often with blood. 

C. Acute proliferative glomerulitis 

Most common type may be of two forms: 

1. Intracapillary form: The entire tuft is consider­ably enlarged and occupies the entire capsular space. The capillary loose are free of blood, due to swelling and proliferation of the capillary endothelium. Occasionally, a few polymorphs may be observed in the capillary loops and interstitial connective tissue. 

2. Extracapillary or subcapsular form: Swelling or proliferation of the epithelium underlying the cap­sule of Bowman. The mass of cells may form a circular rim around the glomeruli or a crescentic mass. 

SUBACUTE GLOMERULONEPHRITIS

Gross Appearance 
(Large white kidney) 

1.  Enlarged, slightly or considerably 
2.  Capsule strips easily 
3.  Exposed surface is smooth and pale. 

Cut Surface 

1.  Marked swelling and pallor of the cortex 
2.  Pyramids unusually dark 
3.  Consistence soft. 

Microscopic Appeamnce 

1.  Glomeruli enlarged 3-4 times; without blood. 
2.  Thickening of the capillary basement membrane (membranous glomerulonephritis). 
3. Erythrocytes, desquamaed epithelium, albu­min and fibrin aceumulato in subcapsular space; usually confined to one part (epithelial crescent). 
 
Fig. 9.1. Acute proliferative glomerulonephritis 
1. Glomeruli lose circular shape 
2. Tufts encroaching the tubules 
3. Increased cellularity
Fig. 9.2. Subacute glomerulonephritis Fig. 9.3. Chronic glomerulonephritis
4. Degenerative changes in the tubules due to lack of blood supply to medullary portion. 
5. Cloudy swelling, fatty degeneration, or necrosis in convoluted tubules. 
6. Collections of small round cells in the interstital tissue. 

CHRONIC GLOMERULONEPHRITIS

Gross Appearance 

1.  Size initially normal; later shrunken with granular surface. 
2.  Red, pale or mottled with yellow foci. 
3.  Cuts with increased resistance. 

Cut Surface 
1.  Flat; in advanced cases retracts and is firm 
2.  Cortex narrowed; striations obscure 
3.  Border between cortex and medulla ill-defined 
4.  Glomeruli mostly white 
5.  Medulla narrowed but less than cortex 
6.  Peripelvic fat increased in amount 
7.  Pelvic mucosa normal 
8.  Arteries often sclerotic. 

Microscopic Appearance 

1.  Renal archetecture completely lost. 
2.  Some glomeruli show extreme hyalinisation. 
3. Several glomeruli atrophic and shrunken but their capillaries still allow passage of some blood. 
4.  Other glomeruli hypertrophied. 
5.  Convoluted tubules show extreme degree of atrophy. 
6. Some tubules appear normal or more often are dilated and lined by high epithelium with papillary buds projecting into the lumen; when dilatation is marked, the cells become low or even flattened. 
7. Interstitial tissue increased. 
8. Arteries supplying the fibrosed, atrophic areas show fibrous thickening of intima causing gArrpydgg of lumen (disuse atrophy). 

PYELONEPHRITIS

Etiology 

Causative Organisms 
1. Escherichia coli (50%) 
2. Aerobacter aerogenes 
3. Proteus vulgaris 
4. Pseudomonas pyocyanea 
5. Coagulase positive staphylococci 
6. Haemolytic streptococci 
7. Enterococci. 
 

Modes of Infection 

1.  Ascent from below in: 
 (i) Infancy 
 (ii) Pregnancy 
(iii) Old persons - due to prostatic enlarge­ment, cancer of cervix and uterine prolapse. 

2. Haernatogenous. 

Predisposing Factors 

1. Diabetes mellitus 
2. Previous parenchymatous damage 
3. Urethral obstruction. 

Gross Appearance 

The lesions may be local or diffuse. The changes vary with the stage of the disease. 

A. In acute stage 
1. Kidney swollen and congested 
2. Pelvis bright red and filled with pus 
3. Yellow spots under the capsule representing areas of suppuration. 

Cut Surface 
1. Patching areas of suppuration; spherical in cortex and linear in pyramids. 
2. If suppuration is progressive, abscess cavities form with gradual destruction of renal tissue. 
3. Outline of calyces destroyed 

B. In chronic cases 
1.  Little frank suppuration. 
2. Inflammation extends in scattered areas destroying the renal tissue but followed by healing, fibrosis and contraction (contracted granular kidney). 
3. The depressed scars on the surface tend to be dark and saddle shaped, appearing U-shaped on cut surface. 
 
Fig. 9.4. Acute pyelonephritis (Late stage : Fibrosis developing)
Fig. 9.5. Chronic pyelonephritis
Microscopic Appearance 
1. Small abscesses with widespread interstitial infiltration of streaky linear round cells and polymorphs. 
2. Renal tubules, destroyed and replaced by scar tissue. 
3. Many tubules, especially in the scarred areas, are lined by flattened epithelium and filled with dense, acidophilic colloid like material. 
4. Periglomerular fibrosis is marked even when the glomeruli are intact. 
5. Round cell infiltration or fibrosis in the renal pelvis. 
6.  Arteries in the affected areas show endarterities obliterans. 

HYDRONEPHROSIS

Causes of Hydronephrosis 

A. Intrinsic 

1.  Congenital: 
(i)  Abnormalities in the posterior urethra 
(ii)  Valve-like mucosal folds at pelviureteric junction 

2. Acquired: 
(a) In the ureter: (i) Calculus (ii) Stricture (iii) Kinking (iv) Accidental ligature. 

(b)  In the bladder: 
 (i) Calculus 
 (ii) Spasm of internal sphincter. 

(c)  In the urethra 
 -Stricture urethrae. 

B. Extrinsic: 
(i) Pelvic tumours 
(ii) Enlarged prostate 
(iii)  Aberrant branch of renal artery pressing the ureter. 

Gross Appearance 

1. Pelvis and calyces are greatly dilated. 
2. Pyramids are destroyed first, followed by cortex until kidney is finally converted into a thin walled lobulated bag of watery fluid. 
3. The greatly distended calyces are separated by incomplete septa. 
4. Ischaemia produced by the pressure of re­tained fluid causes destruction of the renal parenchyma. 
5. If infection is superimposed the walls of the sac become thicker and the lining more rough. 

Hydronephrotic fluid is relatively sterile as continuous circulation is maintained by: 
1.  Pyelovenous back-flow from the minor calyces into the straight veins at the base of pyramids. 
2.  Pyelotubular back-flow which increases with dilatation of the tubular system. 
3.  Possibly the lymphatic channels also. 

Microscopic Appearance 

1.  Initially only tubular atrophy; glomeruli normal. 
2. Later, glomeruli are fibrosed and renal parenchyma is reduced by fibrous tissue 
3. Even in advanced cases, glomeruli as well as tubules in some areas appear fairly normal. 

Complications 

1. Hypertension 
2. Uraemia leading to death. 

ARTERIOLAR NEPHROSCLEROSIS

Types of Nephrosclerosis 

1.  Benign hypertensive nephroscierosis 
2.  Malignant hypertensive nephrosclerosis 
3.  Senile nephroscierosis. 

Benign Hypertensive Nephrosclerosis 

Gross Appearance 
(Primary contracted Granular kidney) 
Unevenly granular 
Reduced in size 
Red in colour 
Consistence firm and elastic 
Capsule thickened but not markedly adherent 
On stripping, the surface is mottled and granular. 

On Cut Section 
1.  Cortex atrophied, without normal markings. 
2.  Parenchyma presents a reddish mottling or strippling. 
3.  Arteries thick-walled and prominent, particularly in boundary zone; also more numerous. 
4.  Medulla diminished in thickness but less in proportion to cortex. 
5.  Pelvic fat increased in amount. 

Microscopic Appearance 
1. Cortex shows areas of fibrosis alternating with less affected areas. 
2. Walls of the intralobular arteries are sclerotic; may show fatty change. 
3. Intima of small arterioles greatly swollen, hyaline and contains much fat. 
4. Glomeruti irregularly arranged in the connective tissue around the arteries. 
5. Tubules atrophied; lined with small cuboidal cells. 
6. Fibrous tissue contains patches of lymphocytic infiltration. 
7. Colloid casts in the connecting tubules. 
8. Larger arteries show hypertrophic changes and fibrosis. 

Malignant Hypertensive Nephrosclerosis 

Gross Appearance 
1. Size normal or slightly diminished 
2.  Surface uneven with reddish spots due to congestion and haemorrhage. 

On Cut Section 
1.  Reddish areas in the cortex, running perpendicularly. 
2.  Renal artery and branches show marked sclerosis. 

Microscopic Appearance 

1. Patches of interstitial change (cellular and fibrotic). 
2. Small arteries show great intimal thickening due to concentric layers of connective tissue; lumina much dilminished. 
3. Arterioles show hyaline and fatty change in intima; fibrinoid necrosis in the walls. 
4.  Necrosis may extend to the roots of glomerufi. 
5.  Glomeruli show irregular and intense capillary congestion with haemorrhage in the space. 
6.  Secondary proliferation of capsular epithethelium may follow. 

Senile Nephrosclerosis 

Gross Appearance 
1. Kidneys small in size 
2. Capsule thickened and adherent 
3. Depressed areas with finely granular surface 
4. Certain portions show extreme atrophy 
5. On cut section. Cortex in depressed areas may be reduced to a mere line, while in the other parts it is less affected. 

Microscopic Appearance 
1. Groups of sclerosed glomeruli irregularly drawn together. 
2. Tubules Atrophied, with propotionately less overgrowth of connective tissue. 
3. At places without atrophy, renal tissue may be relatively unaffected; the preceding changes are observed in atrophied areas only. 
4.  Atheroma is commonly present in large arteries. 

Causes of Contracted Granular Kidney 

1. Benign hypertensive nephrosclerosis 
2. Senile nephrosclerosis 
3. Chronic glomerulonephritis 
4. Chronic pyelonephritis 
5. Polyarteritis nodosa 
6. Diabetes meUitus. 

Gross Appearance 
1.  Glistening, greyish yellow flecks beneath the capsule and deeper in the cortex. 
2.  These foci project from the cut surface giving the appearance of shining grains of sand. 
3.  In later stages, these flecks may be associated with small irregular scars. 

Microscopic Appearance 
1. Spherical nodules of interstitial inflammatory cells which invaginate the wall of a tubule into its lumen. 
2. The infiltrate consists of histiocytes, lympho­cytes, and rarely plasma cells along with a few eosinophils. 
3. Cholesterol crystals, in the tubular lumen, amidst Epid macrophages, other mononuclear cells, polymorphs and cellular debris. 
4. Glomeruli and tubules atrophied only in inflammatory areas;  normal otherwise. 

Haemosiderosis and Haemoglobinuric Nephrosis 
Paroxysmal cold hamoglobinuria is a rare disorder which occurs chiefly in congenital syphilis. There is haemosiderosis of proximal tubules. Kidney function remains unaffected. 
 

RENAL SYPHILIS

Syphilitic Lesions in the Kidney 

1. Congenital interstitial nephritis 
2. Gumma 
3. Syphilitic nephrosis 
4.  Focal interstitial nephritis 
5.  Haemosiderosis and haemoglobinuric nephrosis. 

Congenital Interstitial Nephritis 

The kidney of congenital syphilis is characterised by interstitial inflammation in association with great numbers of treponemas in the interstitial spaces, in the tubular lumen and among the tubular epithelial cells. 

Gumma 
1.  Syphilitic gumma of the kidney is rarely seen 
2.  The histology is that of gumma in other organs 
3. It is probable that multiple irregular scars in the kidn6ys of syphilitic individuals are the healed gummas. 

Syphilitic Nephrosis 

1.  Manifests as sudden onset of nephrotic syndrome, without renal insufficiency. 
2.  Usually in the secondary stage of syphilis. 

Syphilitic Focal Interstitial Nephritis 

Asymptomatic damage to the kidney in secondary stage of syphilis. 

RENAL CALCULI

Structure of Renal Calculi 

The calculus consists of a nucleus of organic matter around which urinary salts are deposited in concentric layers which are bound together by a colloid matrix of organic matter. The salts, al­though crystalline in the urine, are in the form of amorphous granules in the calculus. The calculi may consist of. 
1.  Uric acid and urate 
2.  Calcium oxalate 
3.  Calcium and ammonio-magnesium phosphate. 

Mode of Formation 
The following factors are held responsible for the formation of renal calculi. 

1. Infection. Infection is important in the secondary phosphate stone which is a common consequence of cystitis associated with enlarge­ment of the prostate. It is probable that a mild infection is the starting point of all the uric acid and oxalate stones in the kidney, although, it is not readily detected like the gross infection which is responsible for the secondary phosphate stones. The type of the stone depends upon the reaction of the urine and that depends upon infection. A uric acid or oxalate stone is formed when the urine is acidic. Infection with pyogenic cocci turns the urine alkaline and the stone becomes coated with phosphate. Subsequent infection with Esch. coli may bring back an acidic reaction with deposition of uric acid or calcium oxalate. 

2. Concentration of the crystalline salts. The relation of colloids of the urine to the crystalloids is probably of great importance. The presence of an abnormal colloid or absence of a normal one may cause crystalloids to be precipitated, especially if they are present in excess. 

3. Parathyoid tumour. This is commonly associated with bilateral and recurring calculi. As a result of hyper-parathyroidism, calcium is removed from the bones, the blood is flooded with calcium and this tends to be deposited in the renal pelvis. Such stones have high content of calcium and phosphates. 

4. Vitamin A deficiency. Lack of this vitamin leads to keratinization and desquamation of the epithelium of the renal pelvis which may form the nidus for a stone. It also affects the urinary colloids so that they fail to hold the crystalloids in solution. 

5. Nephrocalcinosis. The term refers to the depo­sition of calcium and phosphorus in the renal tubules or in the interstitial tissue of the kidney. The condition is characterized by hypercalcinuria, negative calcium balance and evidence in skiagram. It is often associated with the formation of calculi. 

6. Prolonged immobility. When patients such as paraplegics are confined to bed for long periods unable to move their limbs, the bones tend to become decalcified and phosphate stones are often formed. 

DIABETIC NEPHROPATHY

Diabetic Glomerulosclerosis 

The glomerular lesions of diabetic nephropathy are of three types: 
 (i) Nodular 
 (ii) Diffuse 
 (iii) Exudative. 

The nodules are usually situated at the periphery of the affected glomerulus. These are eosinophilic and show a laminated appearance when stained with periodic acid Schiff reagent. The initial lesion probably starts within the capillary wall. The hya­ 
line mass increases in size, projects into and finally obliterates the capillary lumen. There is great variation in size of the nodule in different glomeruli, in their frequency within a single and in their distribution in different parts of the kidney. The nodular lesion is the most characteristic pathological abnormality of the disease but it correlates less with the impairment of the renal function than does the diffuse lesion. 

The diffuse glomerular lesion is more common than the nodular lesion and is the main cause of the reduced glomerular filtration rate and azotaemia characteristic of the later stages of diabetic glomerulosclerosis. The capillary walls are thickened by deposit of a substance rich in polysacharide. The basement membrane is probably first involved, with later extension to endothelial and epithelial cells. In the earlier stages, the changes are uneven within the same glomerulus and in different parts of the kidney. Later the whole glomerulus becomes hyalinised and bloodless and there is atrophy of the corresponding tubule. The diffuse lesion may occur without any evidence of nodular change but whenever there are nodular lesions, the diffuse change will be present in the other glomeruli. 

The exudative lesion is the least common and least characteristic abnormality of the glomerulus in diabetic nephropathy. It consists of an eosinophilic structureless crescentic area surrounding the periphery of a lobule of a glomerulus. It stains more 
strongly eosinophilic than the nodular or diffuse lesion. The exudative lesion is only found in the kidneys affected by diffuse glomerulosclerosis, and is a late manifestation of diabetic nephropaihy, usually associated with severe vascular disease elsewhere. 

Other changes in diabetic nephropathy include usually severe renal vascular disease with hyaline change in the wall of arterioles and secondary areas of ischaemic atrophy. Pyelonephritis often occurs in diabetes mellitus especially in the later stages of diabetic nephropathy. Distal tubular or papillary necrosis is of frequent occurrence. 

ACUTE RENAL FAILURE

I. Pre-renal Causes: 

1. Circulatory failure: (i) Cardiac (ii) Peripheral 
(iii) Occlusion of renal vessels. 

2. Severe fluid and electrolyte imbalance 
3. Allergies and over-whelming toxaemias 
4. Addisonian crisis. 

II. Renal Causes: 

1. Acute glomerulonephritis 
2. Anoxic tubular nephrosis 
3. Toxic tubular nephrosis 
4. Acute pyclonephritis 
5. Pyemic kidney 
6. Papillitis necroticans 
7. Bilateral cortical necrosis 
8. Eclampsia 
9. Malignant nephroselerosis 
10. Radiation nephritis. 

III. Post-renal Causes: 

1. Obstruction in ureters 
2. Obstruction in bladder 
3. Obstruction in urethra. 
 

Effects 

Uraemia is associated with headache, drowsiness, twitching of extremities, convulsions, coma and a group of other symptoms and signs. The features disclosed by biopsy are variable, but,there are renal lesions, degenerations of hypertrophic heart, cerebral edema, ulcerative ileocolitis and increased amount of urea in the renal cortex. Often bronchopneumonia is present as a terminal event. 

CHRONIC RENAL FAILURE

Causes 

1.  Glomerulonephritis 

2. Primary tubular disease: 
(i) Fanconi syndrome 
(ii) Renal tubular acidosis 
(iii) Heavy metal poisoning, e.g., lead 
(iv) Phenacetin poisoning. 

3.  Vascular disease: 
 (i) Malignant nephroselerosis 
 (ii) Ischaemic disease of the kidney 
 (iii) Collagen disease 
 (iv) Polyarteritis nodosa 
 (v) Diffuse systemic sclerosis (scleroderma) 
 (vi) Disseminated lupus erythematosus 
(vii) Multiple myelomatosis. 

Infections: (i) Chronic pyelonephritis (ii) Tuberculosis. 

5.  Metabolic renal diseases: 
 (i) Diabetes mellitus 
 (ii) Arnyloidosis 
 (iii) Gout 
 (iv) Hyperparathroidism 
 (v) Milk-alkali syndrome. 

6.  Congenital anomalies of the kidney: 
 (i) Hypoplastic kidneys 
 (ii) Polycystic kidneys. 

7. Urinary tract obstruction: 
 (a) Upper: 
  (i) Calculi 
  (ii) Peri- ureteric fibrosis 
(iii) Neoplasms. 

(b)  Lower: 
 (i) Prostatic enlargement 
 (ii) Stricture urethrae 
(iii)  Congenital anomalies of bladder,  neck, urethra. 

Fanconi Syndrome 

It is a clinical syndrome characterised by: 
 (i) Aminoaciduria 
 (ii) Glycosuria 
 (iii) Proteinuria 
 (iv) Polyuria 
 (v) Low plasma inorganic phosphate 
 (vi) Chronic acidosis 
(vii)  Severe rickets resistant to vitamin D therapy. 

The condition usually becomes apparent in early childhood and death generally occurs before puberty. There is a widespread deposition of cystine in different tissues (cystinosis), the cause of which is not known although it implies a profound 
disturbance in aminoacid metabolism. There is a gross defect in the proximal tubules of the kidney, resulting in imperfect reabsorption of aminoacids, glucose, phosphate, bicarbonate, etc. The proxi­mal tubule is shorter than normal and is joined to 
the glomerulus by a narrow swan like neck. The syndrome is inherited as a mendelian recessive character with no abnormality in the heterozygotes. 

A similar entity generally referred to as adult Fancony syndrome has been found as a familial condition in adults. It is not associated with cystine deposition and presents as a form of osteomalacia. Such biochemical abnormalities as the aminoaciduria and glycosuria may be recognized prior to development of any clinical symptoms. 

NEPHROTIC SYNDROME

The Nephrotic syndrome (or Lipid nephrosis is a clinical complex consisting of :- 

(i)  Proteinuria, principally albuminuria. 
(ii)  Hypoproteinaemia with a reversal of the normal albumin: globulin ratio. 
(iii)  Hypercholesterolaemia. 
(iv)  Lipiduria with oval fat bodies and lipid masses and crystals. 
(v)  Oedema in the form of anasarca and effusions. 

This clinical complex is referred to as pure nephrotic syndrome. It is distinguished from the impure, mixed or complicated nephrotic syndrome in which the following additional features are present: 

(i) Haematuria (ii) Hypertension (iii) Pyuria (iv) Azotaemia. 
 

Etiology 

1. Idiopathic: 
Vast majority of cases. 

2. Systemic disease: 
(i) Diabetes mellitus (ii) Amyloidosis (iii) Systemic lupus erythematosus (iv) Syphilis. 

3. Kidney disorders: 
(i) Chronic glomerulonephritis (ii) Subacute glomerulonephritis (iii) Renal vein thrombosis. 

4. Chemical agents: 
(i) Trimethadione (ii) Gold salts (iii) Mercury (iv) Bee stings (v) Poison oak. 

Vast majority of the cases of nephrotic syndrome are idiopathic. Only rarely the cause is known. The following theories have been forwarded to explain the etiology of idiopathic nephrotic syndrome :- 

(i) A preceding streptococcal infection. In an established case of nephrosis, subsequent recurrent streptococcal infections affect the disease process adversely. 
(ii)  Auto-immune response. Deposition of globulin has been demonstrated in human nephrotic kidney by fluorescent staining techniques. 
(iii)  Chemical toxins. 

Pathogenesis 

Once the glomerular lesion, i.e., abnormality of the epithelial foot processes and subsequent basement membrane thickening, is established, oedema in nephrotic syndrome follows proteinuria. Albumin is the main protein lost though other protein fractions like alpha and gamma globulins also are lost considerably. Proteinuria is mainly responsible for hypoproteinaemia. Protein intake is also low because of accompanying anorexia and diminished absorption of ingested proteins, because of intes­tinal oedema. This may further add to hypoproteinemia. 

Hypoproteinaemia leads to decreased colloidal osmotic pressure allowing escape of water into cellular tissue. This starts the oedema and sets up the factors which contribute further to accumu­lation of fluid in the body. 

The escape of water from plasma leads to reduction of blood volume leading to hormonal disturbances concerned with water and electrolyte regulation. There is increased secretion of antidiuretic hormone (ADH) and aldosterone. Aldosterone retains sodium and alongwith that more and more water is retained. However, the retained water cannot be held in circulation because of hypoproteinaemia and is lost to the extracellular tissue causing further reduction in blood volume and the whole cycle repeats. 

Like the interstitial tissue in all other organs, that of the kidney is also water-logged. This raises intrarenal hydrostatic pressure with its effect on venular patency. This raised internal venular resistance reduces the effective glomerular filtration and also increases tubular water absorption. The tense stretched capsule of the swollen kidney might be responsible for autonomic nerve stimulation causing afferent arteriolar spasm reducing glomerular filtration. 

The cause of hyperchlolesterolaemia is not fully understood. It is believed that it results from increased synthesis of cholesterol and of lipoproteins, and can be induced by certain nephrotoxic sera. 

Chart 9.1. Pathogenesis of nephrotic syndrome

TUMOURS 
Classification 
I. Kidney Proper 
1.  Tumours of renal tubules: 
 (i) Adenoma 
 (ii) Carcinoma. 

2.  Embryonal tumours 
 Wilm's tumours. 

II. Renal Pelvis 
(i)  Papilloma 
(ii) Papillary carcinoma 
(iii) Non-papillary carcinoma. 

Renal Adenoma 

Gross Appearance 
Macroscopic appearance. They are small yellow nodules frequently multiple, usually 1 cm or less in diameter but occasionally large circumscribed but often encapsulated. They arise in areas damaged by vascular occlusion thus appearing as compensatory hyperplasias. 

Microscopic appearance. The tubules may be ir­regular or dilated, papillary processes may project into them. Some of the cells are small, dark or compact, but others may be large clear cells, so as to resemble those of the clear cell carcinoma. The capsule, if at all present may be penetrated by tumour cells. 
 
 
 
 
Fig. 9.6. Papillary adenoma of kidney
Fig. 8.7. Clear-cell carcinoma of kidney.
Fig. 9.8 Wilm's tumour.
Renal Carcinoma (Nephroma) 

Macroscopic appearance. The tumour arises in the upper or lower pole but more often in the middle portion of the kidney. It begins near capsule and enlarges to form a globular mass. Fibrous tissue may form a capsule around the tumour. The tumour is soft and in the cross-section is bulging, o yellow colour, bleeds freely and is often lobulated by fibrous trabeculae. There are numerous foci and masses of necrosis and haemorrhage; the tumour, often, compresses and distorts the pelvis and may invade it. Extension into the tributaries of the renal vein, into the main renal vein and even upto the vena cavae is not infrequent. 

Microscopic appearance. It varies greatly. The most common form is made up of large cuboidal or polyhedral cells with clear vesicular cytoplasm which may contain fat or glycogen. The nuclei are small, fairly dense and often eccentric. These cells grow in bands and papillary projections from a delicate fibrous reticulum. containing many capillaries which may give an alveolated character to the tumour. Necrosis, haemorrhage and blood pigment are common, other tumours are made up of smaller cells with granular cytoplasm and dense, centrally disposed nuclei. In these tumours, the cells are usually in sheets and masses. In either form acini may be found and these are often papilliferous, However, there may be mixtures of these types of cells with preponderance of one or the other. The supporting connective tissue is richly vascularized. 

Metastases are most frequent in lungs, liver, adrenals and bones and less frequent in kidney, spleen, heart and brain. 

Wilm's tuniours (nephroblastoma). This is the commonest malignant tumour of early childhood. It usually occurs during the first three years of life but may rarely occur in adults. It may attain an enormous size, nearly filling the abdomen. Quite 
frequently it is bilateral. There is no haematuria and pain because the renal pelvis is not invaded. 

The tumour, which commences in the cortex, is 2 grey, soft and has a homogeneous character of a sarcoma. It tends to destroy the whole kidney and may spread to neighbouring organs. Distant meta­stases by the blood stream are not frequent. 

 The microscopic appearance varies in different parts of the same tumour. The general character is sarcomatous. The cells may be round or fusiform. Glandular elements are often present; smooth muscle and striated muscle are not uncommon and in rare cases there may be cartilage and bone. 

CONGENITAL DISORDERS
Classification 
A. Abnormalities in the amount of renal tissue 
1. Agenesis 
2. Hypoplasia 
3. Large kidney 
4. Supernumerary kidneys 
B. Abnormalities of position, form and orientation 
1. Displacement of kidneys 
2. Horseshoe kidney. 
C.  Cystic diseases. 
AGENESIS OF KIDNEY

1.  Bilateral agenesis of kidneys is incompatible with life and is found only in still-born babies. 

2. Unilateral agenesis is compatible with adequate renal function. The other kidney is enlarged in size. 

Causes 

1.  Unilateral absence of nephrogenic primordium. 
2.  Failure of Wolffian duct to make contact with mesodermal mass. 

Pathology 
1. There is generally no evidence of kidney. 
2. Occasionally, a small undifferentiated connective tissue mass 2-3 cm in size, may be present. 
3. The renal artery and the renal vein may be absent or rudimentary. 
4. Ureteric remanant may be present. 
5. The functional kidney is enlarged in size (compensatory hypertrophy). 

HYPOPLASIA

Renal hypoplasia means the failure of the kidney to attain the normal size. 
1. It may be bilateral. The patient usually dies during infancy or childhood when infection or stone further reduces renal function. 
2. Oligomeganephroma. The kidney is hypoplastic but the remaining nephrons are markedly hypertrophied. 
 
 

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