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Underweight status increases the risk of cardiovascular disease and mortality in the general population. However, whether underweight status is associated with an increased risk of developing end‐stage kidney disease is unknown. A total of 9 845 420 participants aged ≥20 years who underwent health checkups were identified from the Korean National Health Insurance Service database and analysed. Individuals with underweight (body mass index [BMI] < 18.5 kg/m2) and obesity (BMI ≥ 25 kg/m2) were categorized according to the World Health Organization recommendations for Asian populations. During a mean follow‐up period of 9.2 ± 1.1 years, 26 406 participants were diagnosed with end‐stage kidney disease. After fully adjusting for other potential predictors, the moderate to severe underweight group (<17 kg/m2) had a significantly higher risk of end‐stage kidney disease than that of the reference (normal) weight group (adjusted hazard ratio, 1.563; 95% confidence interval, 1.337–1.828), and competing risk analysis to address the competing risk of death also showed the similar results (adjusted hazard ratio, 1.228; 95% confidence interval, 1.042–1.448). Compared with that of the reference BMI group (24–25 kg/m2), the adjusted hazard ratios for end‐stage kidney disease increased as the BMI decreased by 1 kg/m2. In the sensitivity analysis, sustained underweight status or progression to underweight status over two repeated health checkups, when compared with normal weight status, had a higher hazard ratio for end‐stage kidney disease. Underweight status is associated with an increased risk of end‐stage kidney disease, and this association gradually strengthens as BMI decreases.

Optimal blood pressure (BP) control is a major therapeutic strategy in the management of chronic kidney disease (CKD). We studied the association between BP and adverse kidney outcomes within a diverse cohort of Koreans with CKD.

Incident hemodialysis patients have the highest mortality in the first several months after starting dialysis. This study evaluated the in-hospital mortality rate after hemodialysis initiation, as well as related risk factors.

Despite strong evidence linking decreased glomerular filtration rate (GFR) to worse outcomes, the impact of GFR on mortality and morbidity in patients with acute myocardial infarction (AMI) is not well defined.

It has been shown that the inhibition of the Rho/Rho kinase (ROCK) pathway prevents tubulointerstitial fibrosis and ameliorates renal function in various progressive renal disorders. The present study was to determine whether fasudil, a ROCK inhibitor, has a protective effect on cyclosporine A (CsA)-induced nephropathy. Male Sprague-Dawley rats were treated with CsA (n = 10, 20 mg · kg(-1) day(-1) s.c.), CsA + fasudil (n = 10, 3 mg · kg(-1) day(-1) i.p.), or vehicle alone (n = 10) for 28 days. Fasudil cotreatment ameliorated CsA-induced changes and restored renal function. CsA decreased the expression of endothelial nitric-oxide synthase and increased inducible nitric-oxide synthase/3-nitrotyrosine in the kidney. Accordingly, there was infiltration of inflammatory cells and up-regulation of inflammatory cytokines. Fasudil also significantly suppressed the expression of transforming growth factor-β1, Smad signaling, and subsequent epithelial-to-mesenchymal processes. In addition, fasudil augmented p27(kip1) expression and decreased the number of proliferating cell nuclear antigen-positive cells. In another series of experiments using HK-2 cells in culture, fasudil also suppressed CsA-induced increases in mitogen-activated protein kinase phosphorylation. CsA induced expression of p53, the degree of which was attenuated by fasudil in association with decreases of proapoptotic markers such as Bad, Bax, and total/cleaved caspase-3. These results suggest that inhibition of the Rho/ROCK pathway attenuates CsA-induced nephropathy through the suppression of the induction of inflammatory, apoptotic, and fibrogenic factors, along with inhibition of Smad, mitogen-activated protein kinases, and nitric oxide signaling pathways.

Vitamin D is thought to exert a protective effect on renal disease progression, but the underlying molecular mechanism remains unclear. We investigated whether paricalcitol ameliorates tubular dysfunction and fibrosis in gentamicin (GM)-induced renal injury. Two groups of rats were treated with GM (100 mg·kg−1·day−1), one of which was cotreated with paricalcitol (0.3 μg·kg−1·day−1) for 14 days and the other was not. The control group was treated with vehicle only. HK-2 cells were cultured with GM in the absence or presence of paricalcitol. Paricalcitol restored impaired renal function and the downregulated renal sodium transporters and aquaporin-1 expression caused by GM. ED-1-expressing monocyte/macrophage accumulation induced by GM was attenuated by paricalcitol treatment. Paricalcitol prevented upregulated inflammatory cytokines (TNF-α, IL-1β, INF-γ) and adhesion molecules (monocyte chemoattractant protein-1, ICAM-1, VCAM-1) induced by GM. In addition, paricalcitol effectively reversed TGF-β1-induced epithelial-to-mesenchymal transition (EMT) process and extracellular matrix accumulation in GM-induced nephropathy. Increased collagen deposition and fibrosis in GM-treated kidney were ameliorated by paricalcitol. Paricalcitol also attenuated the upregulated NF-κB and phosphorylated ERK1/2 expression in HK-2 cells cultured with GM. In conclusion, paricalcitol prevents GM-induced renal injury by inhibiting renal inflammation and fibrosis, the mechanism of which is the interruption of NF-κB/ERK signaling pathway and preservation of tubular epithelial integrity via inhibiting EMT process.

We investigated whether -lipoic acid (-LA), an antioxidant, attenuates the ischemia-reperfusion (I/R)-induced dysregulation of these transporters. Both renal pedicles of male Sprague-Dawley rats were clamped for 40 min. -LA (80 mg/kg) was administered intraperitoneally before and immediately after induction of ischemia. After 2 days, the expression of aquaporins (AQPs), sodium transporters, and nitric oxide synthases (NOS) was determined in the kidney by immunoblotting and immunohistochemistry. The expression of endothelin-1 (ET-1) mRNA was determined by real-time PCR. Activities of adenylyl cyclase and guanylyl cyclase were measured by stimulated generation of cAMP and cGMP, respectively. The expression of AQP1–3 as well as that of the 1-subunit of Na-K-ATPase, type 3 Na/H exchanger, Na-K-2Cl cotransporter, and Na-Cl cotransporter was markedly decreased in response to I/R. The expression of type VI adenylyl cyclase was decreased in I/R-injured rats, which was counteracted by the treatment of -LA. AVP-stimulated cAMP generation was blunted in I/R rats and was then ameliorated by -LA treatment. -LA treatment attenuated the downregulation of AQPs and sodium transporters. The expression of endothelial NOS was decreased in I/R rats, which was prevented by -LA. The cGMP generation in response to sodium nitroprusside was blunted in I/R rats, which was also significantly prevented by -LA. The mRNA expression of ET-1 was increased, which was recovered to the control level by -LA treatment. In conclusion, -LA treatment prevents I/R-induced dysregulation of AQPs and sodium transporters in the kidney, possibly through preserving normal activities of local AVP/cAMP, nitric oxide/cGMP, and ET systems.

We investigated whether α-lipoic acid (α-LA), an antioxidant, attenuates the ischemia-reperfusion (I/R)-induced dysregulation of these transporters. Both renal pedicles of male Sprague-Dawley rats were clamped for 40 min. α-LA (80 mg/kg) was administered intraperitoneally before and immediately after induction of ischemia. After 2 days, the expression of aquaporins (AQPs), sodium transporters, and nitric oxide synthases (NOS) was determined in the kidney by immunoblotting and immunohistochemistry. The expression of endothelin-1 (ET-1) mRNA was determined by real-time PCR. Activities of adenylyl cyclase and guanylyl cyclase were measured by stimulated generation of cAMP and cGMP, respectively. The expression of AQP1–3 as well as that of the α1-subunit of Na-K-ATPase, type 3 Na/H exchanger, Na-K-2Cl cotransporter, and Na-Cl cotransporter was markedly decreased in response to I/R. The expression of type VI adenylyl cyclase was decreased in I/R-injured rats, which was counteracted by the treatment of α-LA. AVP-stimulated cAMP generation was blunted in I/R rats and was then ameliorated by α-LA treatment. α-LA treatment attenuated the downregulation of AQPs and sodium transporters. The expression of endothelial NOS was decreased in I/R rats, which was prevented by α-LA. The cGMP generation in response to sodium nitroprusside was blunted in I/R rats, which was also significantly prevented by α-LA. The mRNA expression of ET-1 was increased, which was recovered to the control level by α-LA treatment. In conclusion, α-LA treatment prevents I/R-induced dysregulation of AQPs and sodium transporters in the kidney, possibly through preserving normal activities of local AVP/cAMP, nitric oxide/cGMP, and ET systems.

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Reduced kidney function is associated with an increased risk of cancer; however, it is unclear if cancer increases the risk of kidney failure with replacement therapy (KFRT). We assessed the risk of KFRT among patients with various types of cancer collectively and with specific types of cancer.

A 52-year-old man undergoing continuous ambulatory peritoneal dialysis presented with two consecutive episodes of peritonitis caused by unusual organisms, namely, Brevibacteriumand Pantoea agglomerans. The patient was successfully treated with a 2-week course of cefazolin and ceftazidime for the Brevibacterium-associated peritonitis, and a 3-week course of gentamicin for the P. agglomerans-associated peritonitis. Although these environmental organisms are rarely responsible for human infection, the number of reported cases of human infection by these unusual organisms has increased. This report emphasizes the potential for infection by environmental organisms in patients undergoing peritoneal dialysis.

We report an unusual case of probable Creutzfeldt–Jakob disease (CJD) in hemodialysis patient. A woman 59 years of age with a past history of hypertension and end-stage renal disease presented with a stuporous state preceded by rapidly progressive cognitive dysfunction, myoclonus, and akinetic mutism. At first, the cause of the altered mental status was assumed to be uremic or hypertensive encephalopathy combined with fever. Proper managements, however, did not improve the neurologic symptoms. Diffusion-weighted magnetic resonance imaging revealed bilaterally asymmetric high signal intensity in both basal ganglia and cerebral cortices. Electroencephalography showed diffuse generalized theta-to-delta range slow wave and intermittent medium-to-high voltage complexes with a characteristic triphasic pattern on both hemispheres. Cerebrospinal fluid assay for the 14-3-3 protein was positive and diagnostic of CJD.

Renal vein thrombosis (RVT) is a well-recognized complication of the nephrotic syndrome, but it is extremely rare in patients with acute pancreatitis. Vascular thrombosis complicating pancreatitis is thought to be due to release of proteolytic enzymes from the pancreas and direct vasculitis. Peripancreatic vessels are most commonly involved in the complications associated with pancreatitis. Renal vein and inferior vena cava (IVC) thrombosis, however, is an exceptionally rare complication of pancreatitis. Awareness of this complication will help physicians in its early diagnosis and management. We report a case of renal vein and IVC thrombosis in a patient with acute pancreatitis.

This study was undertakern to examine the protective effects of the aliskiren on gentamicin (GM)-induced nephropathy.

Whether triple antiplatelet therapy is superior to dual antiplatelet therapy for patients with acute myocardial infarction (AMI) and renal dysfunction who underwent percutaneous coronary intervention (PCI) is still unresolved.