Renal Pathophysiology

CHAPTER 11 Acute Kidney Injury


much of an increase each nephron can accommodate, and the threshold for so dium and potassium retention (positive balance) is significantly reduced in the setting of low GFR. Increased ANP, decreased activity of the renin-angiotensin-aldosterone system, and pressure natriuresis due to volume expansion–induced hypertension all may contribute to the decline in sodium reabsorption. (These hormonal systems are reviewed in Chapter 2.) Potassium balance, on the other hand, is maintained by increased collecting tubule potassium secretion. This process is stimulated by a rise in the plasma po tassium concentration and by aldosterone (see Chapter 7). Note that the rate of aldosterone release cannot be predicted in renal disease because it will tend to be suppressed by volume expansion and enhanced by hyperkalemia. 2 The relationship between the plasma creatinine concentration and the GFR can be predicted only in the steady state when creatinine production and excretion are equal, that is, the plasma creatinine concentration is stable. The GFR cannot be predicted the day after surgery because it is not known whether the patient is in a steady state. For example, the GFR could be < 5 mL/min and the plasma creatinine concentration will continue to rise each day because excretion remains below the rate of production. If, however, the plasma creatinine concentration is stable for several days, then the steady state is present. In this setting, the product of the GFR and the plasma creatinine concentration must be constant (see Chapter 1). This product reflects the amount of creatinine filtered and excreted, which, in the steady state, is equal to the relatively constant amount of creatinine produced. Thus, 3 The urinalysis with acyclovir toxicity is often bland (no cells or casts), but the presence of needle-shaped crystals would be highly suggestive of a drug crystal. If these are not seen and a definitive diagnosis was necessary, a renal bi opsy would likely show a precipitate drug obstructing the tubules. 4 In obstruction, as in other renal diseases, the urine output is equal to the difference between the GFR and tubular reabsorption. Complete obstruc tion results in no urine output, but the output is not predictable in patients with partial obstruction. Although the GFR may be markedly reduced (from elevated tubular pressure), tubular reabsorption also may be diminished due to both the adaptations described in the answer to Question 1 and tubular injury induced by the elevated intratubular pressure. Thus, an output of 1,500 mL/day does not ex clude the presence of partial urinary tract obstruction. 5 Reduced sodium chloride reabsorption in the proximal tubule and loop of Henle will increase the delivery of chloride to the macula densa. This will activate the tubuloglomerular feedback system (see Chapter 1), which will lower the nephron filtration rate until macula densa delivery has returned to normal. If this compensatory decline in GFR did not occur, the reabsorptive capacity of the distal and collecting tubules might be overwhelmed, leading to potentially fatal sodium and water losses. Thus, some investigators have called ATN “acute renal success” because systemic hemodynamics are preserved. 4 mg/dL × 20 mL/min = New GFR (mL/min) × 6 mg/dL New GFR = 13.3 mL/min

CHAPTER 11 Acute Kidney Injury

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