Chapter 045. Azotemia and Urinary Abnormalities (Part 3)

Approach to the Patient: Azotemia Once it has been established that GFR is reduced, the physician must decide if this represents acute or chronic renal injury. The clinical situation, history, and laboratory data often make this an easy distinction. However, the laboratory abnormalities characteristic of chronic renal failure, including anemia, hypocalcemia, and hyperphosphatemia, are often also present in patients presenting with acute renal failure. Radiographic evidence of renal osteodystrophy (Chap. 274) would be seen only in chronic renal failure but is a very late finding, and these patients are usually on dialysis. The urinalysis and renal ultrasound can occasionally...
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Chapter 045. Azotemia and Urinary Abnormalities (Part 3) Chapter 045. Azotemia and Urinary Abnormalities (Part 3) Approach to the Patient: Azotemia Once it has been established that GFR is reduced, the physician mustdecide if this represents acute or chronic renal injury. The clinical situation,history, and laboratory data often make this an easy distinction. However, thelaboratory abnormalities characteristic of chronic renal failure, including anemia,hypocalcemia, and hyperphosphatemia, are often also present in patientspresenting with acute renal failure. Radiographic evidence of renal osteodystrophy(Chap. 274) would be seen only in chronic renal failure but is a very late finding,and these patients are usually on dialysis. The urinalysis and renal ultrasound canoccasionally facilitate distinguishing acute from chronic renal failure. Anapproach to the evaluation of azotemic patients is shown in Fig. 45-1. Patientswith advanced chronic renal insufficiency often have some proteinuria,nonconcentrated urine (isosthenuria; isoosmotic with plasma), and small kidneyson ultrasound, characterized by increased echogenicity and cortical thinning.Treatment should be directed toward slowing the progression of renal disease andproviding symptomatic relief for edema, acidosis, anemia, andhyperphosphatemia, as discussed in Chap. 274. Acute renal failure (Chap. 273)can result from processes affecting renal blood flow (prerenal azotemia), intrinsicrenal diseases (affecting small vessels, glomeruli, or tubules), or postrenalprocesses (obstruction to urine flow in ureters, bladder, or urethra) (Chap. 283). PRERENAL FAILURE Decreased renal perfusion accounts for 40–80% of acute renal failure and,if appropriately treated, is readily reversible. The etiologies of prerenal azotemiainclude any cause of decreased circulating blood volume (gastrointestinalhemorrhage, burns, diarrhea, diuretics), volume sequestration (pancreatitis,peritonitis, rhabdomyolysis), or decreased effective arterial volume (cardiogenicshock, sepsis). Renal perfusion can also be affected by reductions in cardiacoutput from peripheral vasodilatation (sepsis, drugs) or profound renalvasoconstriction [severe heart failure, hepatorenal syndrome, drugs such asnonsteroidal anti-inflammatory drugs (NSAIDs)]. True, or effective, arterialhypovolemia leads to a fall in mean arterial pressure, which in turn triggers aseries of neural and humoral responses that include activation of the sympatheticnervous and renin-angiotensin-aldosterone systems and ADH release. GFR ismaintained by prostaglandin-mediated relaxation of afferent arterioles andangiotensin II–mediated constriction of efferent arterioles. Once the mean arterialpressure falls below 80 mmHg, there is a steep decline in GFR. Blockade of prostaglandin production by NSAIDs can result in severevasoconstriction and acute renal failure. Angiotensin-converting enzyme (ACE)inhibitors decrease efferent arteriolar tone and in turn decrease glomerularcapillary perfusion pressure. Patients on NSAIDs and/or ACE inhibitors are mostsusceptible to hemodynamically mediated acute renal failure when blood volumeis reduced for any reason. Patients with bilateral renal artery stenosis (or stenosisin a solitary kidney) are dependent upon efferent arteriolar vasoconstriction formaintenance of glomerular filtration pressure and are particularly susceptible toprecipitous decline in GFR when given ACE inhibitors. Prolonged renal hypoperfusion can lead to acute tubular necrosis (ATN; anintrinsic renal disease discussed below). The urinalysis and urinary electrolytescan be useful in distinguishing prerenal azotemia from ATN (Table 45-2). Theurine of patients with prerenal azotemia can be predicted from the stimulatoryactions of norepinephrine, angiotensin II, ADH, and low tubule fluid flow rate onsalt and water reabsorption. In prerenal conditions, the tubules are intact leading toa concentrated urine (>500 mosm), avid Na retention (urine Na concentration < 20mM/L; fractional excretion of Na < 1%), and UCr/PCr > 40 (Table 45-2). Theprerenal urine sediment is usually normal or has occasional hyaline and granularcasts, while the sediment of ATN is usually filled with cellular debris and dark(muddy brown) granular casts. Table 45-2 Laboratory Findings in Acute Renal Failure Index Prerenal Oliguric Acute Azotemia Renal Failure BUN/PCr Ratio >20:1 10–15:1 Urine sodium (UNa), 40meq/L Urine osmolality, >500 Fractional exc ...