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INTRODUCTION

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 147-1).

TABLE 147-1INITIAL CLINICAL AND LABORATORY DATABASE FOR DEFINING MAJOR SYNDROMES IN NEPHROLOGY

ACUTE RENAL INJURY

Clinical syndrome is characterized by a rapid, severe decrease in glomerular filtration rate (GFR) [rise in serum creatinine and blood urea nitrogen (BUN)], usually with reduced urine output (See CHAP. 148). Extracellular fluid expansion leads to edema, hypertension, and occasionally acute pulmonary edema. Hyperkalemia, hyponatremia, and acidosis are common. Etiologies include ischemia; nephrotoxic injury due to drugs, toxins, or endogenous pigments; sepsis; severe renovascular disease; glomerulonephritis (GN); interstitial nephritis, particularly allergic interstitial nephritis due to medications; thrombotic microangiopathy; or conditions related to pregnancy. Prerenal failure and postrenal failure are potentially reversible causes.

Rapidly Progressive Glomerulonephritis

Defined as a >50% reduction in renal function, occurring over weeks to months. Broadly classified into three major subtypes on the basis of renal biopsy findings and pathophysiology: (1) immune complex–associated, e.g., in systemic lupus erythematosus (SLE); (2) "pauci-immune," associated with antineutrophil cytoplasmic antibodies (ANCA) specific for myeloperoxidase or proteinase-3; and (3) associated with anti–glomerular basement membrane (anti-GBM) antibodies, ...

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