Kidney Function

The renal tubular epithelial cells that line the multiple distinct nephron segments stretching beyond the glomerulus confront the extraordinary daily task of converting 180 L of glomerular filtrate into 1-2 L of urine. Beyond simple reabsorption of solutes and water, nephron epithelial cells respond to and control the overall organismal balance of acid, solutes, fluid, hormones, vitamins, and xenobiotics. Transport functions of these epithelial cells are accomplished by solute-specific transporters and channels that, aided by specific accessory proteins, provide translocation pathways across the permeability barriers posed by the phospholipid bilayer of the plasma membrane. Transepithelial transport depends on the establishment and maintenance of epithelial cell polarity. Insults to epithelial cell polarity, such as ischemic kidney injury, can lead to loss of transport function. Normal nephron function also requires the collective and consecutive efforts of axially heterogeneous nephron segments of differing water permeabilities and energy requirements, expressing distinct profiles of transporters, channels, and other determinants of epithelial permeability. Thus, the effectiveness of diuretics is determined not only by inhibition of specific transporters, but also by the consequences of increased solute delivery to downstream nephron segments.

Background:: Novel treatment strategies are required to reduce the development of acute kidney injury (AKI) in patients undergoing cardiac surgery. In this respect, remote ischemic preconditioning (RIPC), a phenomenon in which transient nonlethal ischemia applied to an organ or tissue protects another organ or tissue from subsequent lethal ischemic injury, is a potential renoprotective strategy.Study Design:: Secondary analysis of 2 randomized trials.Setting & Participants:: 78 consenting selected nondiabetic patients in a university teaching hospital undergoing elective coronary artery bypass graft (CABG) surgery recruited to 2 previously reported randomized studies.Intervention:: RIPC consisted of three 5-minute cycles of right forearm ischemia, induced by inflating a blood pressure cuff on the upper arm to 200 mm Hg, with an intervening 5 minutes of reperfusion, during which time the cuff was deflated. The control consisted of placing an uninflated cuff on the arm for 30 minutes.Outcomes:: AKI measured using Acute Kidney Injury Network (AKIN) criteria, duration of hospital stay, in-hospital and 30-day mortality.Results:: Numbers of participants with AKI stages 1, 2, and 3 were 1 (3%), 3 (8%), and 0 in the intervention group compared with 10 (25%), 0, and 0 in the control group, respectively (P = 0.005). The decrease in AKI was independent of the effect of concomitant aortic valve replacement and cross-clamp times, which were distributed unevenly between the 2 groups.Limitations:: Retrospective analysis of data. More patients in the RIPC group underwent concomitant aortic valve replacement with CABG; although we have corrected statistically for this imbalance, it remains an important confounding variable.Conclusions:: RIPC induced using transient forearm ischemia decreased the incidence of AKI in nondiabetic patients undergoing elective CABG surgery in this retrospective analysis. A large prospective clinical trial is required to study this effect and clinical outcomes in patients undergoing cardiac surgery.

We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic pauci-immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a pauci-immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in pauci-immune crescentic glomerulonephritis may link the underlying CLL to this patient’s glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose pauci-immune crescentic glomerulonephritis.