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Kidney non-tumor

Renal disease-general

Reviewers: Nikhil Sangle, M.D. (see Reviewers page)
Revised: 11 April 2012, last major update April 2012
Copyright: (c) 2003-2012, PathologyOutlines.com, Inc.


● 20% of women get urinary tract infections
● 1% of Americans develop renal stones
● Divided for analytical purposes into diseases of glomeruli, tubules, interstitium and vessels
● Glomerular diseases tend to be immunologically mediated; tubular and interstitial disorders are often due to toxins / infections
● Glomerular and tubular disease affect each other because glomerular disease impairs the tubular blood supply and increases tubular toxins, and tubular disease causes increased intraglomerular pressure

Acute nephritic syndrome


● Grossly visible hematuria, hypertension, azotemia, oliguria, mild edema, red blood cell casts and variable proteinuria (Wikipedia)
● Associated with postinfectious glomerulonephritis, early Lupus, diffuse crescentic and membranoproliferative glomerulonephritis

Acute renal failure


● Abrupt anuria or oliguria with rapidly progressive azotemia identified by increase in BUN or ammonia



● Increased serum BUN (blood urea nitrogen) and creatinine, due to reduced glomerular filtration rate (GFR)
● Causes are prerenal (hemorrhage, shock, congestive heart failure, volume depletion), renal and postrenal (obstruction)

Chronic renal failure


● Azotemia progressing to uremia over a period of years

Stages of chronic renal failure:
● Diminished renal reserve (GFR 50% normal) with normal BUN/Creatinine
● Renal insufficiency: azotemia, anemia, hypertension, polyuria and nocturia
● Renal failure: GFR < 20% normal, kidneys cannot regulate volume of solutes and patient develops edema, metabolic acidosis and hypocalcemia
● End stage renal disease: GFR <5% normal, represents the end stage of various renal diseases

Nephrotic syndrome


● Proteinuria > 3.5 g/day, hypoalbuminemia (serum level < 3 g/dl), hyperlipidemia, lipiduria and severe edema (anasarca)
● Due to derangement in glomerular capillary walls, which leads to increased permeability to plasma proteins, causing massive (non-selective) proteinuria, microhematuria in 50%, hypoalbuminemia and generalized edema (pitting, periorbital and dependent edema), hypertension in up to 25% and thrombotic tendency
● Hyperlipidemia is due to increased lipoprotein synthesis and decreased catabolism
● Lipiduria is due to leakage of lipoproteins with albumin
● Patients are prone to staphylococcus and pneumococcal infections due to loss of immunoglobulins and factor B of complement
● Thrombosis and thromboemboli are due to loss of anticoagulants such as antithrombin III and antiplasmin
● Associated with minimal change disease (more common in children), focal and segmental glomerulosclerosis, membranous glomerulonephritis (more common in adults), systemic disease (SLE, diabetes, amyloidosis) and congenital nephrotic syndrome



● Azotemia plus clinical signs / symptoms (gastroenteritis, peripheral neuropathy, fibrinous pericarditis, secondary hyperparathyroidism); associated with chronic renal failure
● Tubular defects cause polyuria, nocturia and electrolyte disorders; due to diseases directly or indirectly affecting tubular function

End of Kidney non-tumor > Renal disease-general

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