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A case of biopsy-proven chronic kidney disease on progression from acute phosphate nephropathy.

Woo Chul JOO ; Seoung Woo LEE ; Dong Hyuk YANG ; Jee Young HAN ; Moon Jae KIM

Kidney Research and Clinical Practice.2012;31(2):124-127.

Acute phosphate nephropathy (APhN) following oral sodium phosphate solution (OSP) ingestion as a bowel purgative has been frequently reported. It was recently suggested that APhN could progress to chronic kidney disease (CKD) and a history of APhN might be considered as one of the causes of CKD. However, there are few reports proving APhN as a cause of CKD. Here, we report a case of APhN that progressed to CKD, as proven by renal biopsy.
Biopsy ; Eating ; Nephrocalcinosis ; Phosphates ; Renal Insufficiency, Chronic ; Sodium

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Consecutive episodes of peritonitis in a patient undergoing peritoneal dialysis caused by unusual organisms: Brevibacterium and Pantoea agglomerans.

Joon Seok CHOI ; Chang Seong KIM ; Jeong Woo PARK ; Eun Hui BAE ; Seong Kwon MA ; Soo Wan KIM

Kidney Research and Clinical Practice.2012;31(2):121-123.

A 52-year-old man undergoing continuous ambulatory peritoneal dialysis presented with two consecutive episodes of peritonitis caused by unusual organisms, namely, Brevibacterium and 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.
Brevibacterium ; Cefazolin ; Ceftazidime ; Gentamicins ; Humans ; Middle Aged ; Pantoea ; Peritoneal Dialysis ; Peritoneal Dialysis, Continuous Ambulatory ; Peritonitis

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Hemorrhagic fever with renal syndrome and coexisting hantavirus pulmonary syndrome.

Young Min HONG ; Jin Chang MOON ; Hee Chan YANG ; Kyung Pyo KANG ; Won KIM ; Sung Kwang PARK ; Sik LEE

Kidney Research and Clinical Practice.2012;31(2):118-120.

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease with fever, hemorrhage and renal failure caused by hantavirus infection. Hantavirus induces HFRS or hantavirus pulmonary syndrome (HPS). HPS progression to a life-threatening pulmonary disease is found primarily in the USA and very rarely in South Korea. Here, we report a case of HFRS and coexisting HPS.
Fever ; Hantavirus ; Hantavirus Infections ; Hantavirus Pulmonary Syndrome ; Hemorrhage ; Hemorrhagic Fever with Renal Syndrome ; Lung Diseases ; Renal Insufficiency ; Republic of Korea ; Virus Diseases

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Complete remission induced by tacrolimus and low-dose prednisolone in adult minimal change nephrotic syndrome: A pilot study.

Yong Chul KIM ; Tae Woo LEE ; Hajeong LEE ; Ho Suk KOO ; Kook Hwan OH ; Kwon Wook JOO ; Suhnggwon KIM ; Ho Jun CHIN

Kidney Research and Clinical Practice.2012;31(2):112-117.

BACKGROUND: Few clinical trials have examined the replacement of steroids with other immunosuppressive drugs as a primary treatment modality for minimal change disease (MCD) in adults. We studied the efficacy of tacrolimus to induce complete remission (CR) in adults with MCD. METHODS: We enrolled 14 adults with MCD and nephrotic-range proteinuria. All patients were treated with oral tacrolimus 0.05mg/kg twice daily and prednisolone 0.5mg/kg/day. CR was defined as a urine protein to creatinine ratio of<0.2g protein/g creatinine (g/g cr). The primary outcome was cumulative percentage of CR during 16 weeks. RESULTS: The mean urine protein to creatinine ratio at enrollment was 10.9g/g cr (range: 4.2-18.1g/g cr). The trough tacrolimus level was maintained at 5.99+/-2.63ng/mL. CR was achieved by 13/14 (92.8%) patients within 8 weeks. The cumulative CR rate was 7.7% (1/14), 64.2% (9/14), 71.3% (10/14), and 92.9% (13/14) at 1 week, 2 weeks, 4 weeks, and 8 weeks, respectively. The one remaining patient achieved CR at 20 weeks after treatment, who was followed up for a further 4 weeks. The mean time to achieve CR in the 14 patients was 4.64+/-5.11 (1-20) weeks. Three cases suffered adverse events of abdominal pain, diarrhea, or new-onset diabetes mellitus. CONCLUSION: Tacrolimus and low-dose prednisolone therapy induced CR rapidly (71.3% by 4 weeks and 100% by 20 weeks) and effectively in adult patients with MCD.
Abdominal Pain ; Adult ; Corneal Dystrophies, Hereditary ; Creatinine ; Diarrhea ; Humans ; Nephrosis, Lipoid ; Pilot Projects ; Prednisolone ; Proteinuria ; Steroids ; Tacrolimus

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Intravenous albumin for the prevention of contrast-induced nephropathy in patients with liver cirrhosis and chronic kidney disease undergoing contrast-enhanced CT.

Heejung CHOI ; Yoonjung KIM ; Soo Min KIM ; Junam SHIN ; Hye Ryoun JANG ; Jung Eun LEE ; Wooseong HUH ; Yoon Goo KIM ; Ha Young OH ; Dae Joong KIM

Kidney Research and Clinical Practice.2012;31(2):106-111.

BACKGROUND: The purpose of this study was to evaluate the incidence of contrast-induced nephropathy (CIN), and the effect of intravenous albumin for prophylaxis of CIN in patients with liver cirrhosis (LC) and chronic kidney disease (CKD). METHODS: We conducted a retrospective study of 81 subjects with LC and CKD (estimated glomerular filtration rate (eGFR)<60mL/min/1.73m2) who underwent contrast-enhanced computed tomography (CT). Patients received either isotonic sodium bicarbonate solution (3mL/kg for 1h before CT and 1mL/kg/h for 6h after CT) or albumin (20% albumin, 25mL for 1h before CT and 75mL for 6h after CT). CIN was defined as an increase of > or =25% or > or =0.5mg/dL in serum creatinine level. RESULTS: Overall, CIN developed in three patients (3.7%). Of the 81 subjects, 43 received sodium bicarbonate solution and 38 received albumin. Both groups were comparable with regard to age, sex, diabetes mellitus, and baseline eGFR. The albumin group showed a significantly poorer liver function profile. CIN incidence did not differ significantly between the groups: it occurred in one (2.3%) of the 43 subjects receiving sodium bicarbonate and two (5.3%) of the 38 subjects receiving albumin (P=0.6). However, the albumin group showed a significantly smaller increase in body weight (P=0.03). CONCLUSION: The incidence of CIN in patients with LC and CKD undergoing contrast-enhanced CT after preventive measures was relatively low. The incidence of CIN was not significantly different between sodium bicarbonate and albumin groups.
Body Weight ; Creatinine ; Diabetes Mellitus ; Glomerular Filtration Rate ; Humans ; Incidence ; Liver ; Liver Cirrhosis ; Renal Insufficiency, Chronic ; Retrospective Studies ; Sodium Bicarbonate

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TGF-beta-activated kinase-1: New insights into the mechanism of TGF-beta signaling and kidney disease.

Sung Il KIM ; Mary E CHOI

Kidney Research and Clinical Practice.2012;31(2):94-105.

Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that regulates a wide variety of cellular functions, including cell growth, cellular differentiation, apoptosis, and wound healing. TGF-beta1, the prototype member of the TGF-beta superfamily, is well established as a central mediator of renal fibrosis. In chronic kidney disease, dysregulation of expression and activation of TGF-beta1 results in the relentless synthesis and accumulation of extracellular matrix proteins that lead to the development of glomerulosclerosis and tubulointerstitial fibrosis, and ultimately to end-stage renal disease. Therefore, specific targeting of the TGF-beta signaling pathway is seemingly an attractive molecular therapeutic strategy in chronic kidney disease. Accumulating evidence demonstrates that the multifunctionality of TGF-beta1 is connected with the complexity of its cell signaling networks. TGF-beta1 signals through the interaction of type I and type II receptors to activate distinct intracellular pathways. Although the Smad signaling pathway is known as a canonical pathway induced by TGF-beta1, and has been the focus of many previous reviews, importantly TGF-beta1 also induces various Smad-independent signaling pathways. In this review, we describe evidence that supports current insights into the mechanism and function of TGF-beta-activated kinase 1 (TAK1), which has emerged as a critical signaling molecule in TGF-beta-induced Smad-independent signaling pathways. We also discuss the functional role of TAK1 in mediating the profibrotic effects of TGF-beta1.
Apoptosis ; Extracellular Matrix Proteins ; Fibrosis ; Kidney ; Kidney Diseases ; Kidney Failure, Chronic ; MAP Kinase Kinase Kinases ; Negotiating ; Phosphotransferases ; Renal Insufficiency, Chronic ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Wound Healing

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Current concepts of the podocyte in nephrotic syndrome.

Wen Y DING ; Moin A SALEEM

Kidney Research and Clinical Practice.2012;31(2):87-93.

Nephrotic syndrome is a disorder of the glomerular filtration barrier, and central to the filtration mechanism of the glomerular filtration barrier is the podocyte. We are starting to better understand how this cell, with its unique architectural features, fulfils its exact filtration properties. The multiprotein complex between adjacent podocyte foot processes, the slit diaphragm, is essential to the control of the actin cytoskeleton and cell morphology. Many of the proteins within the slit diaphragm, including nephrin, podocin, transient receptor potential-6 channel, and alpha-actinin-4, have been identified via genetic studies of inherited nephrotic syndromes. Signaling from slit diaphragm proteins to the actin cytoskeleton is mediated via the Rho GTPases. These are thought to be involved in the control of podocyte motility, which has been postulated as a focus of proteinuric pathways. Nephrotic syndrome is currently treated with immunosuppressive therapy, with significant adverse effects. These therapies may work in nephrotic syndrome due to specific effects on the podocytes. This review aims to describe our current understanding of the cellular pathways and molecules within the podocyte relevant to nephrotic syndrome and its treatment. With our current knowledge of the cellular biology of the podocyte, there is much hope for targeted therapies for nephrotic syndromes.
Actin Cytoskeleton ; Diaphragm ; Filtration ; Foot ; Glomerular Filtration Barrier ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Nephrotic Syndrome ; Podocytes ; Proteins ; Proteinuria ; rho GTP-Binding Proteins

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Radiocontrast-induced nephropathy in patients with liver cirrhosis and chronic kidney disease.

Sang Kyung JO

Kidney Research and Clinical Practice.2012;31(2):85-86.

No abstract available.
Humans ; Liver ; Liver Cirrhosis ; Renal Insufficiency, Chronic

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Association between vascular access failure and microparticles in hemodialysis patients.

Jung Hwa RYU ; Su Young LIM ; Dong Ryeol RYU ; Duk Hee KANG ; Kyu Bok CHOI ; Seung Jung KIM

Kidney Research and Clinical Practice.2012;31(1):38-47.

BACKGROUND: Vascular access failure, a major cause of morbidity in hemodialysis (HD) patients, occurs mainly at stenotic endothelium following an acute thrombotic event. Microparticles (MPs) are fragments derived from injured cell membrane and are closely associated with coagulation and vascular inflammatory responses. METHODS: We investigated the relationship between levels of circulating MPs and vascular access patency in HD patients. A total of 82 HD patients and 28 healthy patients were enrolled. We used flow cytometry to measure endothelial MPs (EMPs) identified by CD31+CD42- or CD51+ and platelet-derived MPs (PMPs) identified by CD31+CD42+ in plasma samples of participants. Vascular access patency was defined as an interval from the time of access formation to the time of first access stenosis in each patient. MP counts were compared according to access patent duration. RESULTS: The levels of EMP (both CD31+CD42- and CD51+) and CD31+CD42+PMP were significantly higher in patients than in healthy participants. Levels of CD31+CD42-EMP and CD31+CD42+PMP showed a positive correlation. In nondiabetic HD patients, CD31+CD42-EMPs and CD31+CD42+PMPs were more elevated in the shorter access survival group (access survival <1 year) than in the longer survival group (access survival > or = 4 years). CONCLUSION: Elevated circulating EMP or PMP counts are influenced by end-stage renal disease and increased levels of EMP and PMP may be associated with vascular access failure in HD patients.
Blood Platelets ; Cell Membrane ; Constriction, Pathologic ; Endothelial Cells ; Endothelium ; Flow Cytometry ; Humans ; Kidney Failure, Chronic ; Plasma ; Renal Dialysis

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The insulin-like growth factor system in chronic kidney disease: Pathophysiology and therapeutic opportunities.

Youngman OH

Kidney Research and Clinical Practice.2012;31(1):26-37.

The growth hormone-insulin-like growth factor-insulin-like growth factor binding protein (GH-IGF-IGFBP) axis plays a critical role in the maintenance of normal renal function and the pathogenesis and progression of chronic kidney disease (CKD). Serum IGF-I and IGFBPs are altered with different stages of CKD, the speed of onset, the amount of proteinuria, and the potential of remission. Recent studies demonstrate that growth failure in children with CKD is due to a relative GH insensitivity and functional IGF deficiency. The functional IGF deficiency in CKD results from either IGF resistance due to increased circulating levels of IGFBPs or IGF deficiency due to increased urinary excretion of serum IGF-IGFBP complexes. In addition, not only GH and IGFs in circulation, but locally produced IGFs, the high-affinity IGFBPs, and low-affinity insulin-like growth factor binding protein-related proteins (IGFBP-rPs) may also affect the kidney. With respect to diabetic kidney disease, there is growing evidence suggesting that GH, IGF-I, and IGFBPs are involved in the pathogenesis of diabetic nephropathy (DN). Thus, prevention of GH action by blockade either at the receptor level or along its signal transduction pathway offers the potential for effective therapeutic opportunities. Similarly, interrupting IGF-I and IGFBP actions also may offer a way to inhibit the development or progression of DN. Furthermore, it is well accepted that the systemic inflammatory response is a key player for progression of CKD, and how to prevent and treat this response is currently of great interest. Recent studies demonstrate existence of IGF-independent actions of high-affinity and low-affinity-IGFBPs, in particular, antiinflammatory action of IGFBP-3 and profibrotic action of IGFBP-rP2/CTGF. These findings reinforce the concept in support of the clinical significance of the IGF-independent action of IGFBPs in the assessment of pathophysiology of kidney disease and its therapeutic potential for CKD. Further understanding of GH-IGF-IGFBP etiopathophysiology in CKD may lead to the development of therapeutic strategies for this devastating disease. It would hold promise to use of GH, somatostatin analogs, IGFs, IGF agonists, GHR and insulin-like growth factor-I receptor (IGF-IR) antagonists, IGFBP displacer, and IGFBP antagonists as well as a combination treatment as therapeutic agents for CKD.
Axis, Cervical Vertebra ; Carrier Proteins ; Child ; Diabetic Nephropathies ; Humans ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I ; Kidney ; Kidney Diseases ; Proteins ; Proteinuria ; Renal Insufficiency, Chronic ; Signal Transduction ; Somatostatin

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