RENAL DISEASES Flashcards by Kyla Salgado

RENAL DISEASES
CLASSIFICATION (5)

GLOMERULAR DISORDERS
TUBULAR DISORDERS
INTERSTITIAL DISORDERS
RENAL FAILURE
RENAL LITHIASIS

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IMMUNOLOGIC
+Immune system components produce changes and damage to the membranes (deposition of antibodies, trapped circulating immune complexes)

GLOMERULAR DISORDERS

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Glomerular injury: caused by ___

chemical mediators and toxic substances

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SYNDROMES/MANIFESTATIONS THAT INDICATE GLOMERULAR INJURY
* ASYMPTOMATIC:
* SYMPTOMATIC:

ASY: HEMATURIA OR PROTEINURIA
SY: ACUTE NEPHRITIC SYNDROME AND NEPHROTIC SYNDROME

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Increased permeability to plasma proteins (> 3.5 g/day)

NEPHROTIC SYNDROME

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GLOMERULAR DISORDERS
*ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
+Symptoms appear 1-2 weeks following respiratory infections
and 6 weeks after skin infection caused by _____ that contain ____ in the cell wall.

group A Streptococcus (1)
M protein (2)

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+Major cause of nephrotic syndrome in adults

MEMBRANOUS GLOMERULONEPHRITIS

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Causes: immune complex formation in glomerulus or deposition of complement; associated with persistent hepatitis C, autoimmune diseases, and cancer

*MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

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GLOMERULAR DISORDERS
*MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

+Increased cellularity in the subendothelial cells of the
mesangium, causing _____

thickening of the capillary walls and
extremely dense deposits in the GBM

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+ Glomerulus looks normal in light microscopy but there is loss
of podocyte foot processes in electron microscopy

MINIMAL CHANGE DISEASE

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Major cause of nephrotic syndrome in children

MINIMAL CHANGE DISEASE

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+Affects only certain numbers and areas of glomeruli
(sclerosis/scar tissue)

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

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+Deposition of immune complexes containing IgA in the glomerular membrane or in situ formation of immune complexes after deposition of galactose-deficient IgA

IMMUNOGLOBULIN A (IgA) NEPHROPATHY

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Similar pathophysiology and renal presentation with IgA nephropathy BUT…HSP also shows signs of systemic
vasculitis, younger patients, preceding infection, and abdominal complaints

ENOCH-SCHONLEIN PURPURA/IgA VASCULITIS

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+ Progression of previously discussed glomerular disorders
+ Depends on the amount and duration of the damage to the glomerulus

CHRONIC GLOMERULONEPHRITIS

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+Cytotoxic autoantibody (antiglomerular basement membrane
antibody) against the glomerular basement membranes after
viral respiratory infections
+If with lung hemorrhage (Goodpasture’s syndrome)

ANTIGLOMERULAR BASEMENT MEMBRANE DISEASE

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+Causes a granuloma-producing inflammation of the small
blood vessels of the kidney and respiratory system
* MICROSCOPIC POLYANGIITIS: same but w/o granuloma
formation

WEGENER GRANULOMATOSIS/GRANULOMATOSIS WITH POLYANGIITIS

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TESTING for ANCA
+ Common in Churg-Strauss and microscopic polyangiitis

p-ANCA

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TESTING for ANCA
+ Common in Wegener’s

+ c-ANCA: granular pattern throughout the cytoplasm (directed against
proteinase 3)

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+Like Wegener’s but with elevated eosinophils (severe asthma)
+Most accurate test is lung biopsy showing granulomas and eosinophils

EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS/CHURG-STRAUSS VASCULITIS

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+Most common hereditary nephritis
+Inherited disorder of collagen production affecting the GBM

ALPORT SYNDROME

Deposition of amyloid in the glomeruli
* Primary amyloidosis (AL amyloidosis): deposition of Ig light
chains in plasma cell dyscrasias

AMYLOIDOSIS

+ Common autoantibodies: ANA or antinuclear antibody (best screening test) and anti-dsDNA or anti-double stranded DNA
+ Kidney involvement is usually its most serious manifestation
* Microscopic hematuria and proteinuria

SYSTEMIC LUPUS ERYTHEMATOSUS/LUPUS NEPHRITIS

An autoimmune disease in which organs and cells undergo damage initially mediated by tissue-binding autoantibodies and immune complexes followed by destruction mediated by complement activation and release of cytokines/chemokines

SYSTEMIC LUPUS ERYTHEMATOSUS/LUPUS NEPHRITIS (SAME PARIN IKAW JUD)

+Thickening of GBM (due to the loss of heparan sulfate) and expansion of the mesangium due to the accumulation of extracellular matrix

DIABETIC NEPHROPATHY

* May be due to actual damage to tubules (infection or toxic substances) or if a metabolic or hereditary disorder affects the intricate functions of the tubules

TUBULAR DISORDERS

May be due to decreased blood flow that causes lack of oxygen presentation to the tubules or the presence of nephrotoxic substances in the filtrate

ACUTE TUBULAR NECROSIS

+ Generalized failure of tubular reabsorption in PCT + May be inherited, acquired through exposure to toxic agents, or as a complication of multiple myeloma and renal transplant

FANCONI SYNDROME

+ Inability of tubules to secrete adequate hydrogen ions despite normal GFR + Patients have acidosis but unable to produce an acid urine

RENAL TUBULAR ACIDOSIS

inability of the PCT to reabsorb sodium

+ Bartter’s syndrome

excessive sodium reabsorption in the PCT

Gordon’s syndrome

excessive sodium reabsorption in the DCT

+ Liddle’s syndrome

+ Inherited disorder caused by an autosomal mutation in the gene that produces uromodulin + Increased production of abnormal uromodulin

UROMODULIN KIDNEY DISEASE

only protein produced by the kidney

Uromodulin

* URINARY TRACT INFECTION +Lower UTI: ___ and ___ +Upper UTI: ___ and ___

lower: urethritis and cystitis upper: pyelitis and pyelonephritis

85% of UTI is caused by

Gram-negative rods (E. coli, Proteus, Klebsiella, Enterobacter, Pseudomonas)

+ Most frequently occurs because of the ascending movement of bacteria from a lower UTI into the tubules and interstitium

ACUTE PYELONEPHRITIS

+Bacteria multiply in the interstitium and cause acute inflammation +Tubular necrosis +Bacterial toxins and leukocyte enzymes cause the formation of abscess

ACUTE PYELONEPHRITIS

+Persistent inflammation of renal tissue and causes permanent scarring

CHRONIC PYELONEPHRITIS

Cell-mediated immune response that causes damage to the interstitium and renal tubular epithelium (3-21 days after exposure to the offending agent)

ACUTE INTERSTITIAL NEPHRITIS

Occurs when the bacterial flora is disrupted by antibiotics or pH changes

YEAST INFECTIONS

* Renal calculi or kidney stones * Vary in size from barely visible to large, staghorn calculi

NEPHROLITHIASIS

PATHOGENESIS OF STONES * Conditions favoring the formation of renal calculi: (4)

+Chemical concentration or supersaturation of chemical salts in urine +Optimal pH +Urinary stasis +Nucleation or initial crystal formation

NEPHROLITHIASIS 75-85% of calculi are

calcium oxalate or calcium phosphate

NEPHROLITHIASIS accompanied by chronic urinary infections involving urea-splitting bacteria, usually Proteus species

+ Magnesium ammonium phosphate/struvite/staghorn (5%):

NEPHROLITHIASIS food rich in purine and with uromodulin-associated kidney disease

Uric acid (5-10%)

NEPHROLITHIASIS in conjunction with hereditary disorders of cystine metabolism

Cystine (1%)

NEPHROLITHIASIS medication for HIV patients; poor solubility in physiologic pH

Indinavir

+ Sudden loss of renal function caused by sudden decrease in renal blood flow (25%), acute glomerular and tubular disease (65%, 99% of cases is due to ATN), or renal calculi or obstructions (10%, high BCHP equates to low GFR)

Acute Renal Failure

+ One of the most common causes of acute renal failure in children + Commonly occurs after ingestion of meat infected with verocytotoxin-producing E. coli, most often serotype O157: H7

* HEMOLYTIC-UREMIC SYNDROME

+ Progressive loss of renal function caused by an irreversible and intrinsic renal disease and progresses to end-stage renal disease

Chronic Renal Failure