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

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

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

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

Scleroderma renal crisis is defined as rapidly progressive renal failure and/or new onset of malignant hypertension during the course of systemic sclerosis. Most patients show clinical features of malignant hypertension, but there have been several reports of normotensive renal crisis. We have experienced a 63 year old female patients with acute renal failure due to scleroderma renal crisis who did not show the clinical features of malignant hypertension. She had taken steroid for the treatment of degenerative osteoarthritis and gradually developed shortness of breath and edema. Her blood pressure on admission was 150/90 mmHg and easily controlled by diuretics. Renal biopsy showed onion-skin appearance in the interlobular arteries with varying degree of tubulointerstitial changes. Her renal function rapidly deteriorated despite ACE inhibitor therapy and cytotoxic therapy had to be initiated because of progressive interstitial pneumonitis and myocarditis. We describe a patient with scleroderma renal crisis who did not show the clinical features of malignant hypertension following steroid treatment.
Acute Kidney Injury ; Arteries ; Biopsy ; Blood Pressure ; Diuretics ; Dyspnea ; Edema ; Female ; Humans ; Hypertension, Malignant* ; Lung Diseases, Interstitial ; Middle Aged ; Myocarditis ; Osteoarthritis ; Renal Insufficiency ; Scleroderma, Systemic

BACKGROUND: Hyporesponsiveness to erythropoietin is an important issue in the treatment of the anemia of chronic renal failure. We tried to identify the factors of erythropoietin responsiveness in chronic renal failure patients undergoing maintenance hemodialysis for the effective treatment of anemia. METHODS: Seventy hemodialysis patients with hemoglobin increment over 2.0 g/dL during erythropoietin treatment were divided into two groups by median erythropoietin dose, 120 IU/kg/week (the low-dose group vs. the high-dose group). We compared age, gender, cause of renal failure, duration of hemodialyis, use of angiotensin-converting enzyme inhibitor, hemoglobin, hematocrit, serum iron, TIBC, transferrin saturation, ferritin, albumin, cholesterol, parathyroid hormone (iPTH), CRP, CO2 content, BUN, creatinine and Kt/V between the two groups. RESULTS: The low-dose group had significantly shorter duration of hemodialysis (40.9 months vs. 66.1 months, p=0.036), higher serum albumin level (3.93 g/dL vs. 3.72 g/dL, p=0.011) and lower iPTH level (94.97 pg/mL vs. 218.52 pg/mL, p=0.013) compared with the high-dose group. Serum creatinine level and Kt/V showed a tendency to be higher in the low-dose group but there were no significant differences (10.53 mg/dL vs. 9.40 mg/dL, p=0.053 and 1.69 vs. 1.38, p=0.080). Other clinical and laboratory parameters were not different between the two groups. CONCLUSION: Adequate nutritional support and prevention of secondary hyperparathyroidism may be helpful to enhance the responsiveness of erythropoietin in chronic renal failure patients undergoing maintenance hemodialysis.
Anemia ; Cholesterol ; Creatinine ; Erythropoietin* ; Ferritins ; Hematocrit ; Humans* ; Hyperparathyroidism ; Hyperparathyroidism, Secondary ; Iron ; Kidney Failure, Chronic* ; Nutritional Support ; Parathyroid Hormone ; Renal Dialysis* ; Renal Insufficiency ; Serum Albumin ; Transferrin