Journal Detail Information

1

Cite

Share

Fibrillary glomerulonephritis combined with chronic inflammatory demyelinating polyneuropathy.

Woo Kyung SUNG ; Jin Uk JEONG ; Ki Tae BANG ; Jong Ho SHIN ; Ji Hyung YOO ; Nak Min KIM ; Jun Hyung PARK ; Joo Heon KIM

Kidney Research and Clinical Practice.2015;34(2):117-119. doi:10.1016/j.krcp.2014.10.008

A 58-yr-old man presented with leg edema and subacute weakness of his bilateral lower extremities. Urinary and serum immunoelectrophoresis revealed the presence of lambda-type Bence Jones proteins. He was ultimately diagnosed with monoclonal gammopathy of undetermined significance (MGUS). A renal biopsy specimen showed fibrillary glomerulonephritis (FGN), which was randomly arranged as 12-20 m nonbranching fibrils in the basement membranes. Immunofluorescence studies were negative for immunoglobulin (Ig)G, IgM, IgA, C3, and kappa light chains in the capillary walls and mesangial areas. A Congo red stain for amyloid was negative. Electromyography and nerve conduction velocity examinations results were compatible with the presence of demyelinating polyneuropathy. This case showed a rare combination of FGN, without Ig deposition, and MGUS combined with chronic inflammatory demyelinating polyneuropathy (CIDP).
Amyloid ; Basement Membrane ; Bence Jones Protein ; Biopsy ; Capillaries ; Congo Red ; Edema ; Electromyography ; Fluorescent Antibody Technique ; Glomerulonephritis* ; Immunoelectrophoresis ; Immunoglobulin A ; Immunoglobulin M ; Immunoglobulins ; Leg ; Lower Extremity ; Monoclonal Gammopathy of Undetermined Significance ; Neural Conduction ; Paraproteinemias ; Polyneuropathies*

2

Cite

Share

A rare case of hyperoxaluria presenting with acute liver injury and stone-free kidney injury.

Si Eun KIM ; Seon Jae KIM ; Seong Taek CHU ; Seung Hee YANG ; Yon Su KIM ; Ran Hui CHA

Kidney Research and Clinical Practice.2015;34(2):113-116. doi:10.1016/j.krcp.2014.09.006

A 49-year-old woman visited the clinic because of acute hepatitis and acute kidney injury with decreased urine output presenting microscopic hematuria and proteinuria. An abdominal computed tomography revealed a localized, hypoattenuated lesion in a hepatic lateral segment, and kidney biopsy showed oxalate crystal deposition with tubular necrosis. In addition, the patient's 24-hour urinary excretion of oxalate was increased. Her kidney and liver injury improved after sessions of hemodialysis, and urinary oxalate excretion was normalized. Major mutations in primary hyperoxaluria have not been proven. A full sequencing of target genes may be helpful to diagnose a rare form of primary hyperoxaluria.
Acute Kidney Injury ; Biopsy ; Female ; Hematuria ; Hepatitis ; Humans ; Hyperoxaluria* ; Hyperoxaluria, Primary ; Kidney* ; Liver* ; Middle Aged ; Necrosis ; Proteinuria ; Renal Dialysis

3

Cite

Share

Does hypokalemia contribute to acute kidney injury in chronic laxative abuse?.

Eun Young LEE ; Hyaejin YOON ; Joo Hark YI ; Woon Yong JUNG ; Sang Woong HAN ; Ho Jung KIM

Kidney Research and Clinical Practice.2015;34(2):109-112. doi:10.1016/j.krcp.2014.10.009

Prolonged hypokalemia from chronic laxative abuse is recognized as the cause of chronic tubulointerstitial disease, known as "hypokalemic nephropathy," but it is not clear whether it contributes to acute kidney injury (AKI). A 42-year-old woman with a history of chronic kidney disease as a result of chronic laxative abuse from a purging type of anorexia nervosa (AN-P), developed an anuric AKI requiring hemodialysis and a mild AKI 2 months later. Both episodes of AKI involved severe to moderate hypokalemia (1.2 and 2.7 mmol/L, respectively), volume depletion, and mild rhabdomyolysis. The histologic findings of the first AKI revealed the remnants of acute tubular necrosis with advanced chronic tubulointerstitial nephritis and ischemic glomerular injury. Along with these observations, the intertwined relationship among precipitants of recurrent AKI in AN-P is discussed, and then we postulate a contributory role of hypokalemia involved in the pathophysiology of the renal ischemia-induced AKI.
Acute Kidney Injury* ; Adult ; Anorexia Nervosa ; Female ; Humans ; Hypokalemia* ; Necrosis ; Nephritis, Interstitial ; Renal Dialysis ; Renal Insufficiency, Chronic ; Rhabdomyolysis

4

Cite

Share

Intra-abdominal hypertension does not predict renal recovery or in-hospital mortality in critically ill patients with acute kidney injury.

Hyo Jeong CHANG ; Jihyun YANG ; Sun Chul KIM ; Myung Gyu KIM ; Sang Kyung JO ; Won Yong CHO ; Hyoung Kyu KIM

Kidney Research and Clinical Practice.2015;34(2):103-108. doi:10.1016/j.krcp.2015.03.004

BACKGROUND: Although emerging evidence suggests that intra-abdominal hypertension (IAH) is a predictor of the development of acute kidney injury (AKI), it remains unclear whether the presence of IAH is a predictor of prognosis in patients with AKI. The purpose of this study was to assess whether the presence of IAH could predict prognosis in critically ill patients with AKI. The prognostic value of urinary biomarkers was also determined. METHODS: In this prospective observational study, we enrolled 57 patients with established AKI, who were admitted to the intensive care unit between February 2012 and June 2014. IAH was defined as a sustained elevation in intra-abdominal pressure of > or =12 mmHg, in three consecutive measurements performed daily on the first 3 days. Urinary neutrophil gelatinase-associated lipocalin (NGAL), liver-type fatty acid-binding protein, and simplified acute physiology score II score at the time of admission were also examined. RESULTS: IAH was observed in 78.9% of patients. The in-hospital mortality was 21.1%, and renal recovery during hospitalization was achieved in 40.4% of patients. Although high urinary NGAL [odds ratio (OR), 1.015] and liver-type fatty acid-binding protein (OR, 1.003) were found to be independent predictors of renal recovery, IAH was not. High urinary NGAL (OR, 1.003) and a high simplified acute physiology score II score (OR, 1.102) were independent predictors of in-hospital mortality, while IAH or urinary liver-type fatty acid-binding protein was not. CONCLUSION: Although IAH is prevalent in critically ill patients with AKI, it did not predict AKI prognosis. However, urinary NGAL was found to be a useful predictor of both renal recovery and in-hospital mortality.
Acute Kidney Injury* ; Biomarkers ; Critical Illness* ; Hospital Mortality* ; Hospitalization ; Humans ; Intensive Care Units ; Intra-Abdominal Hypertension* ; Lipocalins ; Neutrophils ; Observational Study ; Physiology ; Prognosis ; Prospective Studies

5

Cite

Share

Changes in serum magnesium concentration after use of a proton pump inhibitor in patients undergoing percutaneous coronary intervention.

Sang Ho PARK ; Sun Hyo LEE ; Ji Sung LEE ; Won Yong SHIN ; Hyo Wook GIL ; Jong Oh YANG ; Eun Young LEE ; Sae Yong HONG

Kidney Research and Clinical Practice.2015;34(2):98-102. doi:10.1016/j.krcp.2015.03.001

BACKGROUND: Although cross-sectional studies have suggested a relationship between proton pump inhibitor (PPI) use and hypomagnesemia, no large-scale cohort study has been conducted to date. Here, we examined the changes in serum magnesium levels in response to PPI use. We hypothesized that PPI use might change the serum magnesium concentration. METHODS: Of the 2,892 patients hospitalized for percutaneous coronary intervention between January 2007 and May 2012, 1,076 patients with normal baseline (1.6-2.5 mg/dL) and follow-up serum magnesium concentrations were enrolled. These patients were divided into two groups: the PPI group and the control group. RESULTS: The mean follow-up period was 9.51+/-2.94 months. The incidence of hypomagnesemia (<1.6 mg/dL) was 0.4% (3/834) in the PPI group and 0.4% (1/242) in the control group (P = 0.904). The change in magnesium levels did not differ between the two groups, and this result was maintained in the analysis of covariance after adjusting for confounding factors (P = 0.381). Moreover, magnesium levels did not significantly differ between the long-term (duration of use > or =12 months, n = 71) and short-term PPI groups (duration of use <12 months, n = 763), and the control group (n = 242; P = 0.620). The effect of PPI use on change in serum magnesium concentration was affected by the use of multiple diuretics (-0.01+/-0.25 mg/dL; P = 0.025), although a single diuretic use with PPI did not alter the change in magnesium level (0.12+/-0.27 mg/dL). CONCLUSION: Changes in magnesium levels might be subtle after PPI use in patients with normal baseline magnesium values.
Cohort Studies ; Diuretics ; Follow-Up Studies ; Humans ; Incidence ; Magnesium* ; Percutaneous Coronary Intervention* ; Proton Pumps*

6

Cite

Share

Transforming growth factor-beta receptor 2 gene polymorphisms are associated with end-stage renal disease.

Hye Jin KI ; Se Yun KIM ; Sang Ho LEE ; Ju Young MOON ; Kyung Hwan JEONG ; Tae Won LEE ; Chun Gyoo IHM ; Su Kang KIM ; Joo Ho CHUNG ; Sun Woo KANG ; Tae Hee KIM ; Yeong Hoon KIM ; Yang Gyun KIM

Kidney Research and Clinical Practice.2015;34(2):93-97. doi:10.1016/j.krcp.2015.05.002

BACKGROUND: Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine involved in immune disorders, cancer, asthma, lung fibrosis, and chronic kidney disease, and its signal pathways are considered crucial mediators of a variety of cellular processes. In addition, several recent studies have reported that TGF-beta receptor (TGF-betaR) gene polymorphism is associated with chronic kidney disease. However, the association between end-stage renal disease (ESRD) and the TGF-beta gene polymorphism has not been sufficiently investigated. In this study, we hypothesized that polymorphisms of the TGF-beta ligands or their receptors may be related to ESRD. METHODS: We assessed the relationship between four single-nucleotide polymorphisms (SNPs) in the TGF-betaR2 and TGF-beta2 genes and ESRD, in 312 patients with ESRD and 258 controls. RESULTS: Compared with the control participants, the frequencies of the TGF-betaR2 (rs764522*C) and TGF-betaR2 (rs3087465*G) alleles were significantly higher in the patients with ESRD. Genotyping analysis demonstrated that two SNPs in TGF-betaR2 of the four SNPs included in the study were significantly associated with ESRD in the codominant 1 [rs764522, odds ratio (OR)=1.65; rs3087465, OR=1.63], dominant (rs764522, OR=1.63; rs3087465, OR=1.57), and log-additive (rs764522, OR=1.54; rs3087465, OR=1.39) models after adjusting for age and sex. CONCLUSION: We suggest that TGF-betaR2 polymorphisms (rs764522 and rs3087465) increase the risk of development of ESRD.
Alleles ; Asthma ; Fibrosis ; Humans ; Immune System Diseases ; Kidney Failure, Chronic* ; Ligands ; Lung ; Odds Ratio ; Polymorphism, Single Nucleotide ; Receptors, Transforming Growth Factor beta ; Renal Insufficiency, Chronic ; Signal Transduction ; Transforming Growth Factor beta ; Transforming Growth Factor beta2

7

Cite

Share

Effect of aldosterone on epithelial-to-mesenchymal transition of human peritoneal mesothelial cells.

Mina YU ; Hyun Soo SHIN ; Hyeon Kook LEE ; Dong Ryeol RYU ; Seung Jung KIM ; Kyu Bok CHOI ; Duk Hee KANG

Kidney Research and Clinical Practice.2015;34(2):83-92. doi:10.1016/j.krcp.2015.03.005

BACKGROUND: Peritoneal fibrosis is one of the major causes of technical failure in patients on peritoneal dialysis. Epithelial-to-mesenchymal transition (EMT) of the peritoneum is an early and reversible mechanism of peritoneal fibrosis. Human peritoneal mesothelial cells (HPMCs) have their own renin-angiotensin-aldosterone system (RAAS), however, it has not been investigated whether aldosterone, an end-product of the RAAS, induces EMT in HPMCs, and which mechanisms are responsible for aldosterone-induced EMT. METHODS: EMT of HPMCs was evaluated by comparing the expression of epithelial cell marker, E-cadherin, and mesenchymal cell marker, alpha-smooth muscle actin after stimulation with aldosterone (1-100nM) or spironolactone. Activation of extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) and generation of reactive oxygen species (ROS) were assessed by western blotting and 2',7'-dichlorofluororescein diacetate staining, respectively. The effects of MAPK inhibitors or antioxidants (N-acetyl cysteine, apocynin, and rotenone) on aldosterone-induced EMT were evaluated. RESULTS: Aldosterone induced EMT in cultured HPMCs, and spironolactone blocked aldosterone-induced EMT. Aldosterone induced activation of both ERK1/2 and p38 MAPK from 1 hour. Either PD98059, an inhibitor of ERK1/2, or SB20358, an inhibitor of p38 MAPK, attenuated aldosterone-induced EMT. Aldosterone induced ROS in HPMCs from 5 minutes, and antioxidant treatment ameliorated aldosterone-induced EMT. N-acetyl cysteine and apocynin alleviated activation of ERK and p38 MAPK. CONCLUSION: Aldosterone induced EMT in HPMCs by acting through the mineralocorticoid receptor. Aldosterone-induced generation of ROS followed by activation of ERK, and p38 MAPK served as one of the mechanisms of aldosterone-induced EMT of HPMCs.
Actins ; Aldosterone* ; Antioxidants ; Blotting, Western ; Cadherins ; Cysteine ; Epithelial Cells ; Humans ; p38 Mitogen-Activated Protein Kinases ; Peritoneal Dialysis ; Peritoneal Fibrosis ; Peritoneum ; Phosphotransferases ; Protein Kinases ; Reactive Oxygen Species ; Receptors, Mineralocorticoid ; Renin-Angiotensin System ; Spironolactone

8

Cite

Share

Pathogenesis of endothelial cell dysfunction in chronic kidney disease: a retrospective and what the future may hold.

Michael S GOLIGORSKY

Kidney Research and Clinical Practice.2015;34(2):76-82. doi:10.1016/j.krcp.2015.05.003

Cardiovascular complications dominate the landscape of chronic kidney diseases (CKD). Endothelial cell dysfunction (ECD) is a well-known culprit of cardiovascular morbidity and it develops in CKD with remarkable frequency. This brief overview of ECD in CKD scans two decades of studies performed in my laboratory, from genetic analyses to proteomic and metabolomics screens. I provide a detailed description of findings related to the premature senescence of endothelial cells, cell transition from the endothelial to mesenchymal phenotype, and stages of development of ECD. Clinical utility of some of these findings is illustrated with data on laser-Doppler flowmetry and imaging in patients with CKD. Some currently available and emerging therapeutic options for the management of ECD are briefly presented.
Aging ; Endothelial Cells* ; Humans ; Laser-Doppler Flowmetry ; Metabolomics ; Phenotype ; Renal Insufficiency, Chronic* ; Retrospective Studies*

9

Cite

Share

Nonimmunologic targets of immunosuppressive agents in podocytes.

Tae Hyun YOO ; Alessia FORNONI

Kidney Research and Clinical Practice.2015;34(2):69-75. doi:10.1016/j.krcp.2015.03.003

Proteinuria is a characteristic finding in glomerular diseases and is closely associated with renal outcomes. In addition, therapeutic interventions that reduce proteinuria improve renal prognosis. Accumulating evidence has demonstrated that podocytes act as key modulators of glomerular injury and proteinuria. The podocyte, or glomerular visceral epithelial cell, is a highly specialized and differentiated cell that forms interdigitated foot processes with neighboring podocytes, which are bridged together by an extracellular structure known as the "slit diaphragm" (SD). The SD acts as a size- and charge-selective barrier to plasma protein. Derangement of SD structure or loss of SD-associated protein results in podocyte injury and proteinuria. During the past decades, several immune-modulating agents have been used for the treatment of glomerular diseases and for the reduction of proteinuria. Interestingly, recent studies have demonstrated that immunosuppressive agents can have a direct effect on the SD-associated proteins and stabilize actin cytoskeleton in podocyte and have therefore introduced the concept of nonimmunologic mechanism of renoprotection by immunomodulators. This review focuses on the evidence that immuno-modulating agents directly target podocytes.
Actin Cytoskeleton ; Epithelial Cells ; Foot ; Immunologic Factors ; Immunomodulation ; Immunosuppressive Agents* ; Nephrotic Syndrome ; Plasma ; Podocytes* ; Prognosis ; Proteinuria

10

Cite

Share

Increased intra-abdominal pressure in acute kidney injury: a cause or an effect?.

Jung Eun LEE

Kidney Research and Clinical Practice.2015;34(2):67-68. doi:10.1016/j.krcp.2015.05.001

No abstract available.
Acute Kidney Injury*

DISPLAY OPTIONS

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share