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

Infliximab is a chimeric anti-tumor necrosis factor-alpha monoclonal antibody. Infusion related reactions and infection are well known side effects of infliximab; however, renal complications have not been well recognized. We report on a patient with late onset-acute tubulointerstitial nephritis (ATIN) after treatment with infliximab and mesalazine for Crohn's disease. A 25-year-old woman was admitted with a purpuric rash on both lower extremities and arthralgia. She had been diagnosed with Crohn's disease 5.6 years previously and had been treated with mesalazine and infliximab. Serum creatinine level, last measured one year ago, was elevated from 0.6 mg/dL to 1.9 mg/dL. Results of urinalysis, ultrasound, and serologic examinations were normal. With a tentative diagnosis of Henoch-Schonlein purpura, oral prednisolone was given, and serum creatinine decreased to 1.46 mg/dL, but was elevated to 2.6 mg/dL again at two months after discontinuation of prednisolone. Renal biopsy indicated that ATIN was probably induced by drug, considering significant infiltration of eosinophils. Concomitant use of infliximab with mesalazine was supposed to trigger ATIN. Oral prednisolone was administered, and serum creatinine level showed partial recovery. Thus, ATIN should be suspected as a cause of renal impairment in Crohn's disease even after a long period of maintenance treatment with infliximab and mesalazine.
Adalimumab/therapeutic use ; Anti-Inflammatory Agents/therapeutic use ; Creatine/blood ; Crohn Disease/*drug therapy ; Drug Therapy, Combination ; Eosinophils/immunology ; Female ; Humans ; Infliximab/*adverse effects/*therapeutic use ; Kidney/pathology ; Mesalamine/*adverse effects/*therapeutic use ; Nephritis, Interstitial/*diagnosis/drug therapy/*etiology ; Prednisolone/therapeutic use

Cryptococcus neoformans is a fungus that causes opportunistic infections in immunocompromised hosts. Skin lesions are found in 10-20% of systemic cryptococcal infections, usually secondary to cryptococcemia, while primary cutaneous cryptococcosis with cryptococcemia is very rare. We report a case of rapidly spreading cryptococcal cellulitis in a 64-year-old male on maintenance hemodialysis taking steroids for encapsulated peritoneal sclerosis. Bluish bullous cellulitis developed on the left forearm and spread rapidly to the other forearm. We identified C. neoformans in the blood and skin lesions. We treated him successfully with liposomal amphotericin B and fluconazole for 15 months. We also review the literature.
Amphotericin B ; Cellulitis* ; Cryptococcosis ; Cryptococcus neoformans* ; Fluconazole ; Forearm ; Fungi ; Humans ; Immunocompromised Host ; Male ; Middle Aged ; Opportunistic Infections ; Peritoneal Fibrosis ; Renal Dialysis* ; Skin ; Steroids