Chapter 045. Azotemia and Urinary Abnormalities (Part 7)

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. A family history of renal failure is often present in patients with hereditary nephritis, and patients with thin basement...
Nội dung trích xuất từ tài liệu:
Chapter 045. Azotemia and Urinary Abnormalities (Part 7) Chapter 045. Azotemia and Urinary Abnormalities (Part 7) Isolated microscopic hematuria can be a manifestation of glomerulardiseases. The RBCs of glomerular origin are often dysmorphic when examined byphase-contrast microscopy. Irregular shapes of RBCs may also occur due to pHand osmolarity changes produced along the distal nephron. There is, however,significant observer variability in detecting dysmorphic RBCs. The most commonetiologies of isolated glomerular hematuria are IgA nephropathy, hereditarynephritis, and thin basement membrane disease. IgA nephropathy and hereditarynephritis can lead to episodic gross hematuria. A family history of renal failure isoften present in patients with hereditary nephritis, and patients with thin basementmembrane disease often have other family members with microscopic hematuria.A renal biopsy is needed for the definitive diagnosis of these disorders, which arediscussed in more detail in Chap. 277. Hematuria with dysmorphic RBCs, RBCcasts, and protein excretion >500 mg/d is virtually diagnostic ofglomerulonephritis. RBC casts form as RBCs that enter the tubule fluid becometrapped in a cylindrical mold of gelled Tamm-Horsfall protein. Even in theabsence of azotemia, these patients should undergo serologic evaluation and renalbiopsy as outlined in Fig. 45-2. Isolated pyuria is unusual since inflammatory reactions in the kidney orcollecting system are also associated with hematuria. The presence of bacteriasuggests infection, and white blood cell casts with bacteria are indicative ofpyelonephritis. White blood cells and/or white blood cell casts may also be seen intubulointerstitial processes such as interstitial nephritis, systemic lupuserythematosus, and transplant rejection. In chronic renal diseases, degeneratedcellular casts called waxy casts can be seen in the urine. Broad casts are thought toarise in the dilated tubules of enlarged nephrons that have undergonecompensatory hypertrophy in response to reduced renal mass (i.e., chronic renalfailure). A mixture of broad casts typically seen with chronic renal failure togetherwith cellular casts and RBCs may be seen in smoldering processes such as chronicglomerulonephritis. ABNORMALITIES OF URINE VOLUME The volume of urine produced varies depending upon the fluid intake, renalfunction, and physiologic demands of the individual. See Azotemia, above, fordiscussion of decreased (oliguria) or absent urine production (anuria). The physiology of water formation and renal water conservation arediscussed in Chap. 272. Polyuria By history, it is often difficult for patients to distinguish urinary frequency(often of small volumes) from polyuria (>3 L/d), and a 24-h urine collection isneeded for evaluation (Fig. 45-4). Polyuria results from two potential mechanisms:(1) excretion of nonabsorbable solutes (such as glucose) or (2) excretion of water(usually from a defect in ADH production or renal responsiveness). To distinguisha solute diuresis from a water diuresis and to determine if the diuresis isappropriate for the clinical circumstances, a urine osmolality is measured. Theaverage person excretes between 600 and 800 mosmol of solutes per day,primarily as urea and electrolytes. If the urine output is >3 L/d and the urine isdilute (diuresis is present. This circumstance could arise from polydipsia, inadequatesecretion of vasopressin (central diabetes insipidus), or failure of renal tubules torespond to vasopressin (nephrogenic diabetes insipidus). If the urine volume is >3L/d and urine osmolality is >300 mosmol/L, then a solute diuresis is clearlypresent and a search for the responsible solute(s) is mandatory. Figure 45-4