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137 APPROACH TO THE PATIENT WITHRENAL DISEASE

137 APPROACH TO THE PATIENT WITHRENAL DISEASE
Harrison’s Manual of Medicine

137

APPROACH TO THE PATIENT WITHRENAL DISEASE

Acute Renal Failure
Chronic Renal Failure
Nephrotic Syndrome
Asymptomatic Urinary Abnormalities
Urinary Tract Infection
Renal Tubular Defects
Hypertension
Nephrolithiasis
Urinary Tract Obstruction
Bibliography

The approach to renal disease begins with recognition of particular syndromes on the basis of findings such as presence or absence of azotemia, proteinuria, hypertension, edema, abnormal urinalysis, electrolyte disorders, abnormal urine volumes, or infection (Table 137-1).

Table 137-1 Initial Clinical and Laboratory Data Base for Defining Major Syndromes in Nephrology

Acute Renal Failure   (See Chap. 138)
Clinical syndrome is characterized by a rapid, severe decrease in GFR (rise in serum creatinine and BUN), usually with reduced urine output. Extracellular fluid expansion leads to edema, hypertension, and occasionally to CHF. Hyperkalemia, hyponatremia, and acidosis are common. Etiologies include ischemia; nephrotoxic injury due to drugs, toxins, or endogenous pigments; sepsis; severe renovascular disease; or conditions related to pregnancy. Prerenal and postrenal failure are potentially reversible causes.
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS   Loss of renal function occurs over weeks to months. Pts are initially nonoliguric and may have recent flulike symptoms; later, oliguric renal failure with uremic symptoms supervenes. Hypertension is common. Pulmonary manifestations range from asymptomatic infiltrates to life-threatening hemoptysis. Urinalysis typically shows hematuria, proteinuria, and RBC casts.
ACUTE GLOMERULONEPHRITIS   (See Chap. 142)   An acute illness with sudden onset of hematuria, edema, hypertension, oliguria, and elevated BUN and creatinine. Mild pulmonary congestion may be present. An antecedent or concurrent infection or multisystem disease may be causative, or glomerular disease may exist alone. Hematuria, proteinuria, and pyuria are usually present, and RBC casts confirm the diagnosis. Serum complement may be decreased in certain conditions.
Chronic Renal Failure   (See Chap. 139)
Progressive permanent loss of renal function over months to years does not cause symptoms of uremia until GFR is reduced to about 10–15% of normal. Hypertension may occur early. Later, manifestations include anorexia, nausea, vomiting, insomnia, weight loss, weakness, paresthesia, bleeding, serositis, anemia, acidosis, and hyperkalemia. Causes include diabetes mellitus, severe hypertension, glomerular disease, urinary tract obstruction, interstitial nephritis. Indications of chronicity include long-standing azotemia, anemia, hyperphosphatemia, hypocalcemia, shrunken kidneys, renal osteodystrophy by x-ray, or findings on renal biopsy.
Nephrotic Syndrome   (See Chap. 142)
Defined as heavy albuminuria (>3.5 g/d in the adult) with or without edema, hypoalbuminemia, hyperlipidemia, and varying degrees of renal insufficiency. Can be idiopathic or due to drugs, infections, neoplasms, multisystem or hereditary diseases. Complications include severe edema, thromboembolic events, infection, and protein malnutrition.
Asymptomatic Urinary Abnormalities
Hematuria may be due to neoplasms, stones, infection at any level of the urinary tract, sickle cell disease, or analgesic abuse. Renal parenchymal causes are suggested by RBC casts, proteinuria, or dysmorphic RBCs in urine. Pattern of gross hematuria may be helpful in localizing site. Hematuria with low-grade proteinuria may be due to benign recurrent hematuria or IgA nephropathy. Modest proteinuria may be an isolated finding due to fever, exertion, CHF, or upright posture. Renal causes include diabetes mellitus, amyloidosis, or other causes of glomerular disease. Pyuria can be caused by UTI, interstitial nephritis, glomerulonephritis, or renal transplant rejection. “Sterile” pyuria is associated with UTI treated with antibiotics, glucocorticoid therapy, acute febrile episodes, cyclophosphamide therapy, pregnancy, renal transplant rejection, genitourinary trauma, prostatitis, cystourethritis, tuberculosis and other mycobacterial infections, fungal infection, Haemophilus influenzae, anaerobic infection, fastidious bacteria, and bacterial L forms.
Urinary Tract Infection   (See Chap. 144)
Generally defined as >105 bacteria per mL of urine. Levels between 102 and 105/mL may indicate infection but are usually due to poor sample collection, especially if mixed flora are present. Adults at risk are sexually active women or anyone with urinary tract obstruction, vesicoureteral reflux, bladder catheterization, neurogenic bladder (associated with diabetes mellitus), or primary neurologic diseases. Prostatitis, urethritis, and vaginitis may be distinguished by quantitative urine culture. Flank pain, nausea, vomiting, fever, and chills indicate kidney infection. UTI is a common cause of sepsis, especially in the elderly and institutionalized.
Renal Tubular Defects   (See Chap. 143)
Generally inherited, they include anatomic defects (polycystic kidneys, medullary cystic disease, medullary sponge kidney) detected in the evaluation of hematuria, flank pain, infection, or renal failure of unknown cause and disorders of tubular transport that cause glucosuria, aminoaciduria, stones, or rickets. Fanconi syndrome is a generalized tubular defect that can be hereditary or acquired, due to drugs, heavy metals, multiple myeloma, amyloidosis, or renal transplantation. Nephrogenic diabetes insipidus (polyuria, polydypsia, hypernatremia, hypernatremic dehydration) and renal tubular acidosis are additional causes.
Hypertension   (See Chap. 124)
Blood pressure >140/90 mmHg affects 20% of the U.S. adult population; when inadequately controlled, it is an important cause of cerebrovascular accident, MI, and CHF and can contribute to the development of renal failure. Hypertension is usually asymptomatic until cardiac, renal, or neurologic symptoms appear. In most cases hypertension is idiopathic and becomes evident between ages 25 and 45.
Nephrolithiasis   (See Chap. 146)
Causes colicky pain, UTI, hematuria, dysuria, or unexplained pyuria. Stones may be found on routine x-ray. Most are radiopaque Ca stones and are associated with high levels of urinary Ca, and/or oxalate excretion, and/or low levels of urinary citrate excretion. Staghorn calculi are large, branching radiopaque stones within the renal pelvis due to recurrent infection. Uric acid stones are radiolucent. Urinalysis may reveal hematuria, pyuria, or pathologic crystals.
Urinary Tract Obstruction   (See Chap. 147)
Causes variable symptoms depending on whether it is acute or chronic, unilateral or bilateral, complete or partial, and on underlying etiology. It is an important reversible cause of unexplained renal failure. Upper tract obstruction may be silent or produce flank pain, hematuria, and renal infection. Bladder symptoms may be present in lower tract obstruction. Functional consequences include polyuria, anuria, nocturia, acidosis, hyperkalemia, and hypertension. A flank or suprapubic mass may be found on physical exam.
Bibliography

For a more detailed discussion, see Part 10: Disorders of the Kidney and Urinary Tract, pp. 1535–1629, in HPIM-15.

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