Renal Pathophysiology



CASE-1 DISCUSSION The patient presented at the beginning of the chapter has hemodynamically mediated AKI. It is important to note that this occurs in the absence of any structural damage to the nephrons and as such is not truly an “injury.” It can be seen without any drop in blood pressure, and a normal urinalysis is seen. This condition results from a combination of factors interfering with the autoregu lation of GFR. At baseline, the patient is on a diuretic and ACE inhibitor, and she has a normal GFR. Two weeks previously, she starts NSAIDs; she is now on medications that affect both afferent and efferent regulation of GFR. Efferent vasoconstriction is inhibited by the ACEi, and NSAIDs block the vasodilatory prostaglandins necessary for afferent vasodilation. GFR is still maintained in this setting as long as there are no additional factors that affect renal blood flow. However, the development of even mild volume depletion from her diarrhea is sufficient, in the setting of both afferent and efferent inhibition of regulation, to lead to a significant drop in GFR (see Fig 1.9). This condition is rapidly reversed with stopping NSAIDs and ACEi (at least temporarily) and correcting the volume depletion with IV fluids. CASE-2 DISCUSSION The patient presented had a fall in urine output and elevations in the BUN and creatinine concentration following major abdominal surgery that was compli cated by episodes of hypotension. The differential diagnosis in this setting is prerenal disease versus ATN. The urinalysis, high urine sodium concentration, high FENa, and urine osmolality of 320 mOsm/kg are all compatible with ATN. The 1.1-mg/dL elevation in the plasma creatinine concentration occurring so soon after surgery suggests that the decline in GFR is relatively severe. It is therefore likely that the great majority of nephrons are poorly functioning or nonfunctioning at the time laboratory tests were obtained. Because the patient is seen in the first few hours after the onset of postisch emic ATN, furosemide (a loop diuretic) is given in an attempt to increase the urine output. Although this will make fluid management of the patient easier, there is no evidence that the administration of diuretics will change the course of recovery. Patients who are oliguric ( < 400 mL of urine per day) have suffered a more severe injury and have a poorer prognosis than patients who are nonoliguric. Increasing urine output with the use of diuretics does not change the prognosis but may make volume management easier. The spontaneous recovery (or increase) in urine output usually precedes improvements in GFR and reductions in serum creatinine.


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1 Sodium balance can be maintained as the GFR falls by lowering the rate of tubular reabsorption. If, for example, the FENa is 0.6% at a normal GFR, then sodium excretion will remain constant at a GFR that is 20% of normal (~ fivefold reduction) if the FENa increases fivefold up to 3%. However, there is a limit to how

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