Gaining a foothold on kidney disease?: The leading cause of kidney disease worldwide is known as focal segmental glomerulosclerosis (FSGS). FSGS is associated with loss of podocytes, an unusual cell type critical for the kidney's blood filtration function. Podocytes form interdigitating foot processes that wrap around capillaries and prevent leakage of plasma proteins into urine (proteinuria). Zhou et al. suppressed proteinuria by preventing podocyte loss in two different rat models of kidney disease, using a compound that selectively inhibits the TRPC5 ion channel (see the Perspective by Chung and Shaw). In short-term studies, this compound had no detectable side effects. Thus, TRPC5 inhibitors may merit exploration as a therapy for progressive kidney disease. Science , this issue p. 1332 ; see also p. 1256

The global prevalence of chronic kidney disease (CKD) is increasing with the aging of populations worldwide. As kidney function declines, the accumulation of metabolic waste products and excessive electrolytes can significantly impair the health of patients with CKD. As nutritional management of patients with CKD is thought to control uremic symptoms and provide beneficial effects on the progression of kidney dysfunction, the diet of patients with CKD should be an important consideration in their care. Many guidelines recommend limiting protein intake in these patients, as high-protein diets aggravate kidney dysfunction. Excess sodium may be associated with CKD progression and all-cause mortality and, therefore, limiting salt intake is generally recommended. Low potassium is associated with muscle weakness and hypertension, whereas high potassium is associated with cardiac arrhythmia. Therefore, recent guidelines recommend adjusting dietary potassium intake on an individual basis to maintain serum potassium levels within the normal range. Appropriate dietary calcium intake is recommended to maintain calcium balance in patients with CKD G3, G4. Given the many dietary considerations for patients with CKD, effective nutritional management is challenging. Individualized strategies are needed to ensure the best outcome for patients with CKD.

Ryu SR, et al. J Korean Med Sci. 2017 Feb;32(2):249-256. https://doi.org/10.3346/jkms.2017.32.2.249

Procalcitonin (PCT) is a useful marker for the diagnosis of systemic inflammatory response syndrome. In addition, PCT is affected by renal function. However, few studies have investigated the relationship between PCT and the development of acute kidney injury (AKI). Hence, we investigated whether serum PCT levels at the time of admission were associated with the development of AKI and clinical outcomes. A total of 790 patients in whom PCT was measured on admission to the intensive care unit (ICU) were analyzed retrospectively. We attempted to investigate whether serum PCT levels measured at the time of admission could be used as a risk factor for the development of AKI in septic and nonseptic patients or as a risk factor for all-cause mortality, and diagnostic usefulness of PCT was further assessed. Serum PCT levels were significantly higher in patients with AKI than in those without AKI (P < 0.001). After multivariable adjustment for clinical factors, laboratory findings, and comorbidities, PCT as a continuous variable showed a significant association with AKI (OR 1.006, 95% CI [1.000–1.011]; P = 0.035). However, PCT was not effective in predicting mortality. The cut-off value of PCT for the prediction of AKI incidence was calculated to be 0.315 ng/ml, with sensitivity and specificity of 60.9% and 56.9%, respectively. The odds ratios (ORs) from an equation adjusted for optimum thresholds of PCT levels for developing AKI with and without sepsis were 2.422 (1.222–4.802, P = 0.011) and 1.798 (1.101–2.937, P = 0.019), respectively. However, there were no absolute differences between the pre- and posttest probabilities after including the PCT value for AKI development. This study suggests that the PCT value was higher in AKI patients than in non-AKI patients, but PCT measurement at the time of admission did not improve the prediction model for AKI.

Chronic kidney disease (CKD) is a major risk factor for the development of cardiovascular disease (CVD). Previous trials have investigated the effects of low-dose aspirin on CVD prevention in patients with diabetes; however, patients with CKD were not examined. The role of aspirin in diabetics is controversial, and the available literature is contradictory. Therefore, we studied whether low-dose aspirin would be beneficial for patients with CKD, a group that is at high risk for CVD. From a total of 25340 patients with CKD, 1884 recipients of low-dose aspirin (100 mg/day) were paired 1∶1 with non-recipients for analysis using propensity score matching. The primary endpoint was the development of atherosclerotic CVD, including coronary arterial disease, stroke, and peripheral arterial disease. Secondary endpoints included death from any cause, bleeding events, doubling of serum creatinine, and renal death. The incidence of a primary endpoint of any atherosclerotic CVD was significantly higher in the aspirin users than in the non-users (P<0.001). Secondary endpoints, including all-cause mortality and composite bleeding events, were not significantly different between the aspirin users and the non-users. However, the doubling of serum creatinine levels (P = 0.001) and renal death (P = 0.042) were significantly associated with the use of aspirin. These results suggest that the use of low-dose aspirin in patients with CKD may have harmful consequences related to the development of CVD and renal progression.