CLS 426 Urine & BodyFluid Analysis

Renal Disease – Part IITubular Disease

Ricki Otten MT(ASCP)SC

uotten@unmc.edu

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Tubular Disease

• Altered tubular function

• Necrosis of tubular epithelium

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Altered Tubular Function

• Caused by– Reabsorption-secretion capability lost– Concentrating-diluting capability lost

• Results in– Build up of waste products in bloodstream– Loss of essential substances into urine

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Altered Tubular Function

• Renal glycosuria– Glucose in urine, renal threshold not exceeded

• Cystinuria

• Cystinosis

• Renal tubular acidosis– Tubules unable to secrete adequate H+ despite

systemic acidosis

Inherited disorders

Cystine crystals in urine

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Urinalysis Findings

• Renal glycosuria: + glucose

• Cystinuria, cystinosis: cystine crystals

• Renal tubular acidosis: pH not as acid as is needed to compensate for systemic acidosis

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Necrosis of Tubular Epithelium

• Destruction of tubular epithelial cells– Toxin– Ischemic event

• Most common cause of renal failure

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Necrosis of Tubular Epithelium

• Clinical presentation: 3 phases– Onset– Renal failure

• Azotemia• Hyperkalemia• Metabolic acidosis• Oliguria

– Recovery

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Acute Tubular Necrosis• Toxic ATN

– Drugs: AminoglycosidesAnestheticsRadiographic dyesChemotherapyAnti-rejection drugs

– Toxins: MercuryLeadCadmiumEthylene glycolPesticidesMushrooms

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Acute Tubular Necrosis

• Ischemic ATN: decreased perfusion of kidneys as a result of hypotensive events

– Sepsis: bacterial infection of bloodstream– Shock– Trauma

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Acute Tubular Necrosis• Urinalysis

– Physical: Yellow, hazy

– Chemical:

Proteinuria (mild), +blood, low specific gravity

– Microscopic:

RBC, WBC, RTE

Casts: RTE, granular, waxy, broad