No abstract available.
Cardiovascular Diseases/*etiology ; Female ; Humans ; Male ; Osteoprotegerin/*blood ; *Renal Dialysis ; Renal Insufficiency, Chronic/*therapy ; *Vascular Stiffness

High dietary protein intake may lead to increased intraglomerular pressure and glomerular hyperfiltration, which in the long-term can lead to de novo or aggravating preexisting chronic kidney disease (CKD). Hence, a low protein diet (LPD, 0.6 to 0.8 g/kg/day) is recommended for the management of CKD. There are evidences that dietary protein restriction mitigate progression of CKD and retard the initiation of dialysis or facilitate incremental dialysis. LPD is also helpful to control metabolic derangements in CKD such as metabolic acidosis and hyperphosphatemia. Recently, a growing body of evidence has emerged on the benefits of plant-dominant low-protein diet (PLADO), which composed of > 50% plant-based sources. PLADO is considered to be helpful for relieving uremic burden and metabolic complications in CKD compared to animal protein dominant consumption. It may also lead to favorable alterations in the gut microbiome, which can modulate uremic toxin generation along with reducing cardiovascular risk. Alleviation of constipation in PLADO may minimize the risk of hyperkalemia. A balanced and individualized dietary approach for good adherence to LPD utilizing various plant-based sources as patients’ preference should be elaborated for the optimal care in CKD. Periodic nutritional assessment under supervision of trained dietitians should be warranted to avoid protein-energy wasting.

High dietary protein intake may lead to increased intraglomerular pressure and glomerular hyperfiltration, which in the long-term can lead to de novo or aggravating preexisting chronic kidney disease (CKD). Hence, a low protein diet (LPD, 0.6 to 0.8 g/kg/day) is recommended for the management of CKD. There are evidences that dietary protein restriction mitigate progression of CKD and retard the initiation of dialysis or facilitate incremental dialysis. LPD is also helpful to control metabolic derangements in CKD such as metabolic acidosis and hyperphosphatemia. Recently, a growing body of evidence has emerged on the benefits of plant-dominant low-protein diet (PLADO), which composed of > 50% plant-based sources. PLADO is considered to be helpful for relieving uremic burden and metabolic complications in CKD compared to animal protein dominant consumption. It may also lead to favorable alterations in the gut microbiome, which can modulate uremic toxin generation along with reducing cardiovascular risk. Alleviation of constipation in PLADO may minimize the risk of hyperkalemia. A balanced and individualized dietary approach for good adherence to LPD utilizing various plant-based sources as patients’ preference should be elaborated for the optimal care in CKD. Periodic nutritional assessment under supervision of trained dietitians should be warranted to avoid protein-energy wasting.

Radiocontrast-induced nephropathy (CIN) is the third most common cause of acute renal failure among inpatients. The number of patients undergoing examinations using radiocontrast is increasing, and the population at risk for CIN is growing; this population includes older individuals and those with underlying diabetes mellitus, chronic kidney disease, hypertensive nephropathy, and concomitant use of nephrotoxic drugs. However, little progress in CIN treatment has been made. CIN remains a substantial medical problem because of its association with prolonged hospitalization, the potential need for renal replacement therapy, and increased mortality. The exact pathogenesis of CIN has not been fully elucidated-and multiple factors including tubular renal vasoconstriction, direct renal tubular toxicity, increased oxidative stress, and cellular apoptosis-may contribute to the proximal tubular damage that occurs in patients with CIN. Despite the exploration of numerous prophylactic regimens and treatments, definite therapeutic and preventive strategies for CIN have not been established. This article reviews recent studies involving the risk factors for CIN as well as its pathophysiology and prevention.
Acute Kidney Injury ; Diabetes Mellitus ; Hospitalization ; Humans ; Inpatients ; Mortality ; Oxidative Stress ; Population Characteristics ; Renal Insufficiency, Chronic ; Renal Replacement Therapy ; Risk Factors ; Vasoconstriction

Paraneoplastic leukocytosis was defined as elevated white blood cell (WBC) levels caused by cytokines, likely produced by the tumor itself, without evidence of infection or myeloproliferative disease. We report a case of anaplastic thyroid carcinoma with leukocytosis caused by elevated production of granulocyte colony-stimulating factor (G-CSF) by the carcinoma. Initially, acute pyelonephritis (APN) was diagnosed and treatment for APN was ongoing, but the WBC count steadily increased to 68.8x10(9)/L. She was diagnosed with anaplastic thyroid carcinoma on her neck mass, and the serum concentration of G-CSF was found to be markedly increased at 1,010 pg/mL. In spite of supportive care, the patient's condition rapidly deteriorated and the patient died on day 23 of hospital stay. Leukocytosis without definite evidence of infection could be a paraneoplastic manifestation in patients with malignant tumors, and paraneoplastic leukocytosis may be related to poor prognosis.
Cytokines ; Granulocyte Colony-Stimulating Factor ; Granulocytes ; Humans ; Length of Stay ; Leukocytes ; Leukocytosis ; Neck ; Prognosis ; Pyelonephritis ; Thyroid Gland ; Thyroid Neoplasms

Paraneoplastic leukocytosis was defined as elevated white blood cell (WBC) levels caused by cytokines, likely produced by the tumor itself, without evidence of infection or myeloproliferative disease. We report a case of anaplastic thyroid carcinoma with leukocytosis caused by elevated production of granulocyte colony-stimulating factor (G-CSF) by the carcinoma. Initially, acute pyelonephritis (APN) was diagnosed and treatment for APN was ongoing, but the WBC count steadily increased to 68.8x10(9)/L. She was diagnosed with anaplastic thyroid carcinoma on her neck mass, and the serum concentration of G-CSF was found to be markedly increased at 1,010 pg/mL. In spite of supportive care, the patient's condition rapidly deteriorated and the patient died on day 23 of hospital stay. Leukocytosis without definite evidence of infection could be a paraneoplastic manifestation in patients with malignant tumors, and paraneoplastic leukocytosis may be related to poor prognosis.
Cytokines ; Granulocyte Colony-Stimulating Factor ; Granulocytes ; Humans ; Length of Stay ; Leukocytes ; Leukocytosis ; Neck ; Prognosis ; Pyelonephritis ; Thyroid Gland ; Thyroid Neoplasms

Neointimal hyperplasia causes vascular stenosis and subsequent thrombosis, which result in vascular access failure in patients undergoing hemodialysis. Interleukin-10 (IL-10) and tumour necrosis factor-alpha (TNF-alpha) are involved in this inflammatory process. The aim of this study was to investigate the relationship between vascular access failure and various inflammatory markers including the genetic polymorphisms of IL-10 and TNF-alpha. Seventy-five patients on hemodialysis with an arteriovenous fistula in place or an artificial graft (18 with vascular access failure and 82 without failure) and 98 healthy individuals were genotyped for IL-10 and TNF-alpha single nucleotide polymorphisms. Clinical and laboratory data including serum IL-10 and TNF-alpha levels were compared. Stimulated IL-10 levels, from in vitro incubation of blood with lipopolysaccharide, were also obtained and compared. Female gender, hypoproteinemia, and hypertriglyceridemia were associated with vascular access failure. The basal TNF-alpha level was significantly higher in patients with access failure. The distribution of IL-10 and TNF-alpha genotype did not differ among patients with or without access failure. This study could not demonstrate a relationship between genetic polymorphisms and vascular access failure. However, an altered immune response and inflammation might contribute to vascular access failure.
Adult ; Aged ; Arteriovenous Shunt, Surgical/*adverse effects ; Catheters, Indwelling/*adverse effects ; Cross-Sectional Studies ; Female ; Humans ; Interleukin-10/blood/*genetics ; Male ; Middle Aged ; *Polymorphism, Single Nucleotide ; *Renal Dialysis ; Tumor Necrosis Factor-alpha/blood/*genetics

BACKGOUND: Renal tubular epithelial cells are primary target for hypoxic injury. Hypoxia induced tubular cell apoptosis has been reported previously and thought to be important mechanism of renal dysfunction in ischemic ARF, but precise signaling mechanisms need to be defined. The aim of this study is to clarify intracellular signaling mechanism mediating apoptosis by hypoxic stimuli in cultured tubular cells. METHODS: HK-2 cells were placed in hypoxic chamber (O2<1%) for 24 hrs in minimal essential medium. DNA fragmentation was detected by Hoechst 33342 stain and FACS. The activation of caspase was measured by fluorometry and activations of p-38, ERK, and JNK were examined by western blot analysis. RESULTS: Hypoxia induced caspase 3 activation and apoptosis at 24 hrs and this was accompanied by increased phosphorylation of p-38, ERK1/2, and JNK. Pretreatment of p-38 inhibitor (SB 203280) and JNK inhibitor (SP600125) did not afftect the activation of caspase 3 and apoptosis but inhibition of ERK1/2 by PD98059 resulted in partial inhibition of caspase 3 and apoptosis induced by hypoxia. CONCLUSION: ERK 1/2 activation can be an upstream signal in hypoxia induced caspase 3 activation and apoptosis in tubular cells.
Anoxia* ; Apoptosis* ; Blotting, Western ; Caspase 3 ; DNA Fragmentation ; Epithelial Cells ; Fluorometry ; Negotiating ; Phosphorylation

PURPOSE: inflammation is a common feature in chronic kidney disease patients, and it could contribute to long-term morbidity and mortality related with malnutrition and atherosclerosis. In this study, we aimed to investigate the effect of initiating dialysis on inflammatory state, nutritional parameter, and immune response in end-stage renal disease (ESRD) patients. METHODS: 57 ESRD patients who initiated hemodialysis (HD, n=31) or continuous ambulatory peritoneal dialysis (CAPD, n=26) were enrolled. Pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, and anti-inflammatory cytokines, interleukin (IL)-10 and adiponectin were measured before and 3 months after initiation of dialysis. Inflammatory marker, highly sensitive C-reactive protein (hs-CRP), and nutritional parameter, albumin, were also checked. Lipopolysaccharide (LPS)-stimulated production of TNF-alpha and IL-10 were measured for the evaluation of immune response by external stimuli. RESULTS: As uremia was reduced by initiating dialysis, serum level of TNF-alpha was decreased and adiponectin was increased. These changes were accompanied by the decrease of hs-CRP and the increase of serum albumin. LPS-stimulated cytokines production was increased after initiating dialysis. There differences in these parameters comparing HD and CAPD patients except more increase of serum adiponectin level in CAPD patients. CONCLUSION: Our study demonstrated that initiation of dialysis results in decrease of inflammation, improvement of nutritional status, and restoration of proper immune responsiveness in ESRD patients. These results suggest that correction of uremic milieu through dialysis has beneficial effects. Therefore, initiation of dialysis might have the advantage of improving inflammatory and nutritional status, and correcting immune dysfunction in ESRD patients.
Adiponectin ; Atherosclerosis ; C-Reactive Protein ; Cytokines ; Dialysis* ; Humans ; Inflammation ; Interleukin-10 ; Interleukins ; Kidney Failure, Chronic* ; Malnutrition ; Mortality ; Nutritional Status ; Peritoneal Dialysis, Continuous Ambulatory ; Renal Dialysis ; Renal Insufficiency, Chronic ; Serum Albumin ; Tumor Necrosis Factor-alpha ; Uremia

Murine typhus is an infectious disease caused by Rickettsia typhi, an intracellular parasite that lives in the cytoplasm of host cells. Rickettsia typhi infection can induce lymphohistiocytic vasculitis leading to pulmonary, cardiovascular, central nervous system and renal complications. We experienced a case of acute renal failure resulting from acute tubulointerstitial nephritis associated with murine typhus infection. A 67 year old man was transferred from local hospital due to fever, confusion, oliguria with renal failure. Laboratory finding showed elevated liver enzyme with hypoalbuminemia and progressive azotemia. Despite supportive care, his azotemia progressed with anuria and acute hemodialysis was started. Kidney biopsy showed acute tubulointerstitial nephritis with vasculitis and indirect immunofluorecent antibody to murine typhus was 1: 3, 200. Doxycyclin was started and his renal function recovered. We report a case of acute renal failure resulting from murine typhus infection induced acute tubulointerstitial nephritis.
Acute Kidney Injury* ; Aged ; Anuria ; Azotemia ; Biopsy ; Central Nervous System ; Communicable Diseases ; Cytoplasm ; Fever ; Humans ; Hypoalbuminemia ; Kidney ; Liver ; Nephritis, Interstitial* ; Oliguria ; Parasites ; Renal Dialysis ; Renal Insufficiency ; Rickettsia typhi ; Typhus, Endemic Flea-Borne* ; Vasculitis