Harrison’s Manual of Medicine



Abnormalities of Renal Function
Abnormalities of Urine Volume
Abnormalities of Urine Composition

Azotemia is the retention of nitrogenous waste products excreted by the kidney. Increased levels of blood urea nitrogen (BUN) (>30 mg/dL) and creatinine (>1.5 mg/dL) are ordinarily indicative of impaired renal function. Renal function can be estimated by determining the clearance of creatinine (CLcr) (normal >100 mL/min). CLcr overestimates glomerular filtration rate (GFR), particularly at lower levels. Isotopic markers (e.g., iothalamate) provide more accurate estimates of GFR.
Manifestations of impaired renal function include: volume overload, hypertension, electrolyte abnormalities (e.g., hyperkalemia, hypocalcemia, hyperphosphatemia), metabolic acidosis, hormonal disturbances (e.g., insulin resistance, functional vitamin D deficiency, secondary hyperparathyroidism), and, when severe, “uremia” (one or more of the following: anorexia, lethargy, confusion, asterixis, pleuritis, pericarditis, enteritis, pruritus, sleep and taste disturbance, nitrogenous fetor).
OLIGURIA   This refers to sparse urine output, usually defined as <400 mL/d. Oligoanuria refers to a more marked reduction in urine output, i.e., <100 mL/d. Anuria indicates the absence of urine output. Oliguria most often occurs in the setting of volume depletion and/or renal hypoperfusion, resulting in “prerenal azotemia” and acute renal failure (Chap. 138). Anuria can be caused by complete bilateral urinary tract obstruction, a vascular catastrophe (dissection or arterial occlusion), renal vein thrombosis, and hypovolemic, cardiogenic, or septic shock. Oliguria is never normal, since at least 400 mL of maximally concentrated urine must be produced to excrete the obligate daily osmolar load.
POLYURIA   Polyuria is defined as a urine output >3 L/d. It is often accompanied by nocturia and urinary frequency and must be differentiated from other more common conditions associated with lower urinary tract pathology and urinary urgency or frequency (e.g., cystitis, prostatism). It is often accompanied by hypernatremia (Chap. 26). Polyuria (Table 25-1) can occur as a response to a solute load (e.g., hyperglycemia) or to an abnormality in antidiuretic hormone (ADH) action. Diabetes insipidus is termed central if due to the insufficient hypothalmic production of ADH and nephrogenic if the result of renal insensitivity to the action of ADH. Excess fluid intake can lead to polyuria, but primary polydipsia rarely results in changes in plasma osmolality unless urinary diluting capacity is impaired, as with chronic renal failure. Tubulointerstitial diseases and urinary tract obstruction can be associated with nephrogenic diabetes insipidus.

Table 25-1 Major Causes of Polyuria

The approach to the pt with polyuria is shown in Fig. 25-1.

FIGURE 25-1. Approach to the patient with polyuria. (OSM, osmolality; ATN, acute tubular necrosis.)

PROTEINURIA   This is the hallmark of glomerular disease. Levels up to 150 mg/d are considered within normal limits. Typical measurements are semi- quantitative, using a moderately sensitive dipstick that estimates protein concentration; therefore, the degree of hydration may influence the dipstick protein determination. Most commercially available urine dipsticks detect albumin and do not detect smaller proteins, such as light chains, that require testing with sulfosalicylic acid. More sensitive assays can be used to detect microalbuminuria in diabetes mellitus. A urine albumin to creatinine ratio >30 mg/g defines the presence of micoalbuminuria.
Urinary protein excretion rates between 500 mg/d and 3 g/d are nonspecific and can be seen in a variety of renal diseases (including hypertensive nephrosclerosis, interstitial nephritis, vascular disease, and other primary renal diseases with little or no glomerular involvement). Lesser degrees of proteinuria (500 mg/d to 1.5 g/d) may be seen after vigorous exercise, changes in body position, fever, or congestive heart failure. Protein excretion rates >3 g/d are termed nephrotic range proteinuria and are accompanied by hypoalbuminemia, hypercholesterolemia, and edema in the nephrotic syndrome. Massive degrees of proteinuria (>10 g/d) can be seen with minimal change disease, primary focal segmental sclerosis, membranous nephropathy, collapsing glomerulopathy, and HIV-associated nephropathy and can be associated with a variety of extrarenal complications (Chap. 142).
Pharmacologic inhibition of ACE or blockade of angiotensin II receptors may reduce proteinuria in some pts, particularly those with diabetic nephropathy. Specific therapy for a variety of causes of nephrotic syndrome is discussed in Chap. 142.
HEMATURIA   Gross hematuria refers to the presence of frank blood in the urine and is more characteristic of lower urinary tract disease and/or bleeding diatheses than intrinsic renal disease (Table 25-2). Cyst rupture in polycystic kidney disease and flares of IgA nephropathy are exceptions. Microscopic hematuria (>1–2 RBC/high powered field) accompanied by proteinuria, hypertension, and an active urinary sediment (the “nephritic syndrome”) is most likely related to an inflammatory glomerulonephritis (Chap. 142).

Table 25-2 Major Causes of Hematuria

Free hemoglobin and myoglobin are detected by dipstick; a negative urinary sediment with strongly heme-positive dipstick are characteristic of either hemolysis or rhabdomyolysis, which can be differentiated by clinical history and laboratory testing. Red blood cell casts are not commonly seen but are highly specific for glomerulonephritis.
The approach to the pt with hematuria is shown in Fig. 25-2.

FIGURE 25-2. Approach to the patient with hematuria. (RBC, red blood cell; WBC, white blood cell; GBM, glomerular basement membrane; ANCA, antineutrophil cytoplasmic antibody; VDRL, venereal disease research laboratory; HIV, human immunodeficiency virus; ASLO, antistreptolysis O; UA, urinalysis; IVP, intravenous pyelography; CT, computed tomography.)

PYURIA   This may accompany hematuria in inflammatory glomerular diseases. Isolated pyuria is most commonly observed in association with an infection of the upper or lower urinary tract. Pyuria may also occur with allergic interstitial nephritis (often with a preponderance of eosinophils), transplant rejection, and noninfectious, nonallergic tubulointerstitial diseases. The finding of “sterile” pyuria (i.e., urinary white blood cells without bacteria) in the appropriate clinical setting should raise suspicion of renal tuberculosis.

For a more detailed discussion, see Denker BM, Brenner BM: Azotemia and Urinary Abnormalities, Chap. 47, p. 262, in HPIM-15.



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