Renal Decapsulation to Treat Ischemic Acute Kidney Injury: A New Twist in an Old Tale*

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In this issue of Critical Care Medicine, Cruces et al (1) provide evidence that renal decapsulation can improve oxygenation and function of the kidney after ischemia. Their findings support the view that the postischemic kidney represents a state of intrinsic renal compartment syndrome. That is, because the renal capsule limits expansion of kidney volume, edema leads to increased renal interstitial hydrostatic pressure (RIHP). In turn, increased RIHP impedes renal perfusion and oxygenation, with the resulting tissue hypoxia perhaps exacerbating functional deficits and structural damage within the kidney (2, 3). Renal decapsulation may, therefore, provide a therapeutic approach to reducing the severity of acute kidney injury (AKI) after renal ischemia. But, this surgical procedure has a long and checkered history.
Renal decapsulation was performed in humans as early as the late 19th century (reviewed in [4]). It was used to treat a wide range of renal diseases, including chronic nephritis, acute glomerulonephritis, and nephrosis among others, with mixed results. It was also used as a treatment for hypertension in the years before development of antihypertensive medications. It seems that this procedure was often followed by relief of pain emanating from the kidneys, but evidence of improved renal function was scant (4, 5). When the procedure enjoyed popularity, the therapeutic efficacy of renal decapsulation was ascribed variously to development of collateral circulations within the kidney, the elimination of toxins that had accumulated under the capsule, “protein shock” from simple handling of the kidney, or destruction of renal sympathetic nerves (4). There was some support for the idea that decapsulation reduces RIHP, but this proposition was often disregarded (4). Perhaps the strongest case for a role of relief of edema was mounted by Reid et al (6) who, in a case of anuria precipitated by transfusion of incompatible blood, observed beneficial effects of renal decapsulation combined with peritoneal dialysis. Regardless, with the dawning of the era of dialysis after the Second World War, this procedure was considered obsolete and so has been rarely employed since (7).
More recent studies of the therapeutic efficacy of renal decapsulation in ischemic AKI have also generated rather conflicting results. In monkeys subjected to various periods of bilateral renal ischemia, the function of, and blood flow to, the decapsulated kidney was found to be uniformly superior to that of the contralateral kidney with an intact capsule (8). Similarly, in a clinical trial of unilateral decapsulation in patients who had suffered from severe hemorrhagic shock, there was evidence of greater blood flow and function of the decapsulated kidney than the kidney with an intact capsule (8). More recently, Herrler et al (9) observed increased RIHP in the days following renal ischemia in mice. Both the elevated RIHP and deficits in renal perfusion were ameliorated by needle puncture of the renal capsule. In contrast, using radioactive microspheres in dogs, others were unable to detect differences in postischemic blood flow between decapsulated kidneys and a contralateral kidney with an intact capsule (10, 11).
The impetus for the current study by Cruces et al (1) came from their previous observations regarding the relationship between the volume of fluid injected into the renal pelvis and RIHP (12). This relationship was nonlinear (exponential) in pigs with an intact renal capsule but linear in pigs in which the renal capsule was removed. Critically, for any given volume of fluid injected into the renal pelvis, the RIHP was considerably less after renal decapsulation. They reasoned that this increase in RIHP should act to limit intrarenal perfusion and thus promote renal tissue hypoxia.
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