Azotemia and urinary abnormalities

Isolated microscopic hematuria can be a manifestation of glomerular diseases. The RBCs of glomerular origin are often dysmorphic when examined by phase-contrast microscopy. Irregular shapes of RBCs may also occur due to pH and osmolarity changes produced along the distal nephron. There is, however, significant observer variability in detecting dysmorphic RBCs. The most common etiologies of isolated glomerular hematuria are IgA nephropathy, hereditary nephritis, and thin basement membrane disease. IgA nephropathy and hereditary nephritis can lead to episodic gross hematuria.

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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; ASLO, antistreptolysin O; UA, urinalysis; IVP, intravenous pyelography; CT, computed tomography. A detailed discussion of glomerulonephritis and diseases of the microvasculature can be found in Chap. 277.

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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.

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Harrison's Internal Medicine Chapter 45. Azotemia and Urinary Abnormalities Azotemia and Urinary Abnormalities: Introduction Normal kidney functions occur through numerous cellular processes to maintain body homeostasis. Disturbances in any of these functions can lead to a constellation of abnormalities that may be detrimental to survival.

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Approach to the patient with polyuria. ATN, acute tubular necrosis; ADH, antidiuretic hormone Excessive filtration of a poorly reabsorbed solute such as glucose, mannitol, or urea can depress reabsorption of NaCl and water in the proximal tubule and lead to enhanced excretion in the urine. Poorly controlled diabetes mellitus with glucosuria is the most common cause of a solute diuresis, leading to volume depletion and serum hypertonicity. Since the urine Na concentration is less than that of blood, more water than Na is lost, causing hypernatremia and hypertonicity.

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The normal glomerular endothelial cell forms a barrier composed of pores of ~100 nm that hold back blood cells but offer little impediment to passage of most proteins. The glomerular basement membrane traps most large proteins (100 kDa), while the foot processes of epithelial cells (podocytes) cover the urinary side of the glomerular basement membrane and produce a series of narrow channels (slit diaphragms) to normally allow molecular passage of small solutes and water but not proteins.

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Assessment of Glomerular Filtration Rate Monitoring the GFR is important in both the hospital and outpatient settings, and several different methodologies are available (discussed below). In most acute clinical circumstances a measured GFR is not available, and the serum creatinine level is used to estimate the GFR in order to supply appropriate doses of renally excreted drugs and to follow short-term changes in GFR. Serum creatinine is the most widely used marker for GFR, and the GFR is related directly to the urine creatinine excretion and inversely to the serum creatinine (U Cr/PCr).

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