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Tubular Diseases



Benign nephrosclerosis Malignant nephrosclerosis
This term is used to describe the changes in kidney associated with benign phase of hypertension This term is used to desribe the changes in kidney associated with malignant or accelerated hypertension
Gross Gross
Kidney size is either normal or may be moderately reduced
Kidney size is variable may be smaller in size (when superimposed on benign nephrosclerosis) or larger in size (enlarged) than normal (patients who develop malignant hypertension in pure form)
Grain leather appearance Flea bitten appearance
The cortical surface has a fine even granularity The cortical surface may show multiple small petechial hemorrhages from rupture of arterioles or glomerular capillaries
Microscopic (vascular changes & parenchymal changes) Microscopic (Vascular changes & parenchymal changes)
Hyaline arteriosclerosis
Fibrinoid necrosis of arterioles (necrotizing arteriolitis)
Narrowing of the lumens of arterioles and small arteries caused by thickening and hyalinization of the walls The vessel wall shows fibrinoid necrosis. Represents an acute event and necrosis is usually not accompanied by intense inflammation
Fibroelastic hyperplasia in the intima (intimal thickening), duplication of elastic lamina and hypertrophy of the 'media'
Hyperplastic intimal sclerosis / onion skinning
Parenchymal changes (due to ischaemic) variable degree of atrophy of parenchyma due to ischemia Concentric laminae of proliferated smooth muscle cells, collagen and basement membrane (producing intimal thickening) Parenchymal changes (due to ischaemia) Variable degree of atrophy of parenchyma due to ischaemia. Infarction necrosis distal to abnormal vessels may be seen

Diseases Affecting Tubules and Interstitium.

  1. Two major groups of processes:
    1. ischemic or toxic tubular injury, leading to acute tubular necrosis (ATN) and acute renal failure, and (2) inflammatory reactions of the tubules and interstitium (tubulointerstitial nephritis)
  2. Acute tubular necrosis
    1. ATN is a clinic pathologic entity characterized morphologically by destruction of tubular epithelial cells and clinically by acute diminution or loss of renal function.
    2. It is the most common cause of acute renal failure, which signifies rapid reduction of renal function and urine flow, falling within 24 hours to less than 400 mL per day.
    3. It can be caused by a variety of conditions, including.
      Ischemia, due to decreased or interrupted blood flow.
      1. Direct toxic injury to the tubules (e.g. by drugs, radiocontrast dyes, myoglobin, hemoglobin, radiation).
      2. Acute tubulointerstitial nephritis, most commonly occurring as a hypersensitivity reaction to drugs.
      3. Urinary obstruction by tumors. 
Pathogenesis. The critical events in both ischemic and nephrotoxic ATN are believed to be
  1. Tubular injury and
  2. Persistent and severe disturbances in blood flow.
Figure : Possible pathogenetic mechanisms in ischemic acute renal failure.
  1. Tubulointerstitial Nephritis
    1. This group of renal diseases is characterized by histologic and functional alterations that involve predominantly the tubules and interstitium.  Q
    2. Chronic tubulointerstitial injury may occur in diseases that primarily affect the glomerulus. 
    3. This secondary tubulointerstitial nephritis is also present in a variety of vascular, cystic (polycystic kidney disease), metabolic (diabetes), and renal disorders, in which is may also contribute to progressive damage. Q

Causes of Tubulointerstitial Nephritis

  1. Infections
    1. Acute bacterial pyelonephritis
    2. Chronic pyelonephritis (including reflux nephropathy)
    3. Other infections (e.g., viruses, parasites)
  2. Toxins
    1. Drugs
    2. Acute hypersensitivity interstitial nephritis
    3. Analgesic nephropathy
    4. Heavy metals
    5. Lead, cadmium
  3. Metabolic Diseases Q
    1. Urate nephropathy
    2. Nephrocalcinosis (hypercalcemic nephropathy)
    3. Hypokalemic nephropathy
    4. Oxalate nephropathy
  4. Physical Factors Q
    1. Chronic urinary tract obstruction
    2. Radiation nephropathy
  5. Neoplasms
    1. Multiple myeloma (cast nephropathy)
  6. Immunologic Reactions Q
    1. Transplant rejection
    2. Sjögren syndrome
    3. Sarcoidosis
  7. Miscellaneous
    1. Balkan nephropathy
    2. Nephronophthisis-medullary cystic disease complex
    3. "Idiopathic" interstitial nephritis
  8. Important features of Tubulointerstitial nephritis
    1. Tubulointerstitial nephritis can be acute or chronic.
    2. Acute tubulointerstitial nephritis has a rapid clinical onset and is characterized histologically by interstitial edema, often accompanied by leukocytic infiltration of the interstitium and tubules, and focal tubular necrosis.
    3. In chronic interstitial nephritis, there is infiltration with predominantly mononuclear leukocytes, prominent interstitial fibrosis, and widespread tubular atrophy.  Q
    4. Morphologic features that are helpful in separating acute from chronic tubulointerstitial nephritis include edema and, when present, eosinophils and neutrophils in the acute form, contrasted with fibrosis and tubular atrophy in the chronic form. Q
Pyelonephritis and Urinary Tract Infection Q
  1. Pyelonephritis is a renal disorder affecting the tubules, interstitium, and renal pelvis and is one of the most common diseases of the kidney.  Q
  2. It occurs in two forms.
  3. Acute pyelonephritis is caused by bacterial infection and is the renal lesion associated with urinary tract infection.  Q
  4. Chronic pyelonephritis is a more complex disorder: bacterial infection plays a dominant role, but other factors (vesicoureteral reflux, obstruction) are involved in its pathogenesis.  Q
  5. Pyelonephritis is a serious complication of an extremely common clinical spectrum of urinary tract infections that affect the urinary bladder (cystitis), the kidneys and their collecting systems (pyelonephritis), or both. 
Acute Pyelonephritis
  1. Acute pyelonephritis is an acute suppurative inflammation of the kidney caused by bacterial and sometimes viral (e.g. polyoma virus) infection, whether hematogenous and induced by septicemic spread or ascending and associated with vesicoureteral reflux. Q
  2. Morphology: The hallmarks of acute pyelonephritis are patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis.
  3. Three complications of acute pyelonephritis are encountered in special circumstances.
    Papillary necrosis
    Perinephric abscess
Chronic pyelonephritis and reflux nephropathy Q
  • Chronic pyelonephritis is a chronic tubulointerstitial renal disorder in which chronic tubulointerstitial inflammation and renal scarring are associated with pathologic involvement of the calyces and pelvis.
  • Chronic pyelonephritis can be divided into two forms: chronic reflux associated and chronic obstructive.
Reflux Nephropathy
  1. Chronic obstructive pyelonephritis
    1. Morphology.
      1. The kidneys usually are irregularly scarred; if bilateral, the involvement is asymmetric.
      2. This contrasts with chronic glomerulonephritis, in which the kidneys are diffusely and symmetrically scarred.
      3. The hallmark of chronic pyelonephritis is the coarse, discrete, corticomedullary scar overlying a dilated, blunted, or deformed calyx. Q
      4. The microscopic changes involve predominantly tubules and interstitium.
      5. The tubules show atrophy in some areas and hypertrophy or dilation in others.
      6. Dilated tubules with flattened epithelium may be filled with colloid casts (thyroidization). 

Xanthogranulomatous pyelonephritis:

  1. Xanthogranulomatous pyelonephritis is a chronic infective condition of the kidney associated with chronic bacterial infection.
  2. The most common organism implicated in causation is proteus followed by E coli (not tuberculosis).
  3. Most of the cases occur in old ages (5th_6th decade), but may occur at any age.
  4. Females are more commonly affected.
  5. Usually involves one kidney (unilateral), but may be bilateral.
  6. Affected kidney, almost always has:
  • Obstruction (large staghorn calculus)
  • Hydronephrosis
Pathological findings
  1. Gross features
  • Enlarged kidney
  • Dilated pelvis
  • Stones of staghorn variety
  • Calyces are typically filled with pus
  • Cortex is studded with yellowish nodules that line the calyces (Granulomatous areas).
  1. Microscopic features
  • Yellow nodules are due to large foam cells (lipid laden histiocytes). Also known as Xanthoma cells.
  • These foam cells contain lipid and PAS positive granules
  • Along with foam cells, lymphocytes, plasma cells and multinucleated giant cells are also present.
  • Lymphoid follicles may be seen.
  • Fibrosis may be seen which may contain foreign body giant cells.
  • Foci of calcification may be seen.

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