Chapter 045. Azotemia and Urinary Abnormalities (Part 4)

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Chapter 045. Azotemia and Urinary Abnormalities (Part 4) Chapter 045. Azotemia and Urinary Abnormalities (Part 4) POSTRENAL AZOTEMIA Urinary tract obstruction accounts for The specific urologic conditions that cause obstruction are discussed inChap. 283. INTRINSIC RENAL DISEASE When prerenal and postrenal azotemia have been excluded as etiologies ofrenal failure, an intrinsic parenchymal renal disease is present. Intrinsic renaldisease can arise from processes involving large renal vessels, intrarenalmicrovasculature and glomeruli, or tubulointerstitium. Ischemic and toxic ATNaccount for ~90% of acute intrinsic renal failure. As outlined in Fig. 45-1, theclinical setting and urinalysis are helpful in separating the possible etiologies ofacute intrinsic renal failure. Prerenal azotemia and ATN are part of a spectrum ofrenal hypoperfusion; evidence of structural tubule injury is present in ATN,whereas prompt reversibility occurs with prerenal azotemia upon restoration ofadequate renal perfusion. Thus, ATN can often be distinguished from prerenalazotemia by urinalysis and urine electrolyte composition (Table 45-2 and Fig. 45-1). Ischemic ATN is observed most frequently in patients who have undergonemajor surgery, trauma, severe hypovolemia, overwhelming sepsis, or extensiveburns. Nephrotoxic ATN complicates the administration of many commonmedications, usually by inducing a combination of intrarenal vasoconstriction,direct tubule toxicity, and/or tubule obstruction. The kidney is vulnerable to toxicinjury by virtue of its rich blood supply (25% of cardiac output) and its ability toconcentrate and metabolize toxins. A diligent search for hypotension andnephrotoxins will usually uncover the specific etiology of ATN. Discontinuationof nephrotoxins and stabilizing blood pressure will often suffice without the needfor dialysis while the tubules recover. An extensive list of potential drugs andtoxins implicated in ATN can be found in Chap. 273. Processes that involve the tubules and interstitium can lead to acute renalfailure. These include drug-induced interstitial nephritis (especially antibiotics,NSAIDs, and diuretics), severe infections (both bacterial and viral), systemicdiseases (e.g., systemic lupus erythematosus), or infiltrative disorders (e.g.,sarcoid, lymphoma, or leukemia). A list of drugs associated with allergicinterstitial nephritis can be found in Chap. 279. The urinalysis usually shows mildto moderate proteinuria, hematuria, and pyuria (~75% of cases) and occasionallywhite blood cell casts. The finding of RBC casts in interstitial nephritis has beenreported but should prompt a search for glomerular diseases (Fig. 45-1).Occasionally renal biopsy will be needed to distinguish among these possibilities.The finding of eosinophils in the urine is suggestive of allergic interstitial nephritisor atheroembolic renal disease and is optimally observed by using a Hansel stain.The absence of eosinophiluria, however, does not exclude these possibleetiologies. Occlusion of large renal vessels including arteries and veins is anuncommon cause of acute renal failure. A significant reduction in GFR by thismechanism suggests bilateral processes or a unilateral process in a patient with asingle functioning kidney. Renal arteries can be occluded with atheroemboli,thromboemboli, in situ thrombosis, aortic dissection, or vasculitis. Atheroembolicrenal failure can occur spontaneously but is most often associated with recentaortic instrumentation. The emboli are cholesterol-rich and lodge in medium andsmall renal arteries, leading to an eosinophil-rich inflammatory reaction. Patientswith atheroembolic acute renal failure often have a normal urinalysis, but the urinemay contain eosinophils and casts. The diagnosis can be confirmed by renalbiopsy, but this is often unnecessary when other stigmata of atheroemboli arepresent (livedo reticularis, distal peripheral infarcts, eosinophilia). Renal arterythrombosis may lead to mild proteinuria and hematuria, whereas renal veinthrombosis typically induces heavy proteinuria and hematuria. These vascularcomplications often require angiography for confirmation and are discussed inChap. 280. Diseases of glomeruli (glomerulonephritis or vasculitis) and the renalmicrovasculature (hemolytic uremic syndromes, thrombotic thrombocytopenicpurpura, or malignant hypertension) usually present with various combinations ofglomerular injury: proteinuria, hematuria, reduced GFR, and alterations of Naexcretion leading to hypertension, edema, and circulatory congestion (acutenephritic syndrome). These findings may occur as primary renal diseases or asrenal manifestations of systemic diseases. The clinical setting and other la ...