Disease relevance of Kidney Diseases

• Familial juvenile nephronophthisis (NPH) is a chronic autosomal recessive kidney disease responsible for 15% of end stage renal failure in children [1].
• The central pathological feature of human kidney disease that leads to kidney failure is the accumulation of extracellular matrix in glomeruli [2].
• By chi-square analysis, only the presence of anti-(H2A-H2B), anti-[(H2A-H2B)-DNA], and antichromatin were correlated with kidney disease measured by proteinuria > 0.5 g/d. SLE patients could be divided into two groups based on their antibody-binding pattern to the above substrates [3].
• Cutting edge: amelioration of kidney disease in a transgenic mouse model of lupus nephritis by administration of the caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-(beta-o-methyl)-fluoromethylketone [4].
• We hypothesized that blocking TGF-beta1 signaling could attenuate renal fibrosis in a rat model of remnant kidney disease [5].

Psychiatry related information on Kidney Diseases

• There was only one case of dementia possibly due to cimetidine (with a drug level of 1.9 microgram/ml 6 hr after a dose) in a group of 13 patients without liver or kidney disease who had cimetidine levels above 1.25 microgram/ml [6].

High impact information on Kidney Diseases

• A new TRP to kidney disease [7].
• Phenacetin abuse is known to produce kidney disease; salicylate use is supposed to prevent cardiovascular disease [8].
• The urinary excretion of N-acetyl-beta-glucosaminidase (NAG) is increased in patients whose renal function is impaired by a variety of kidney diseases, and may provide an index of renal injury [9].
• Mutations in the homeobox gene vHnf1 are associated with human diseases MODY5 (maturity-onset diabetes of the young, type V) and familial GCKD (glomerulocystic kidney disease) [10].
• JAMA patient page. Hypertensive kidney disease [11].

Chemical compound and disease context of Kidney Diseases

• Nine-five patients were free of kidney disease, defined as a creatinine level of less than 1.2 mg/dL (mean, 0.8 mg/dL), and 48 had kidney disease severe enough to raise the plasma creatinine level to 1.5 mg/dL or greater (mean, 6.5 mg/dL) [12].
• Subjects were excluded if they had cardiac, pulmonary, liver, or kidney disease; any impairment in activities of daily living; or steroid use [13].
• Although it is difficult to study angiotensin II-mediated effects in vivo without influencing systemic and glomerular blood pressure, further studies are needed to evaluate the ability of ACE-inhibitors and angiotensin II receptor blockers to suppress TGF-beta overexpression in selected models of chronic progressive kidney disease [14].
• Inhibition of thromboxane synthesis ameliorates the progressive kidney disease of rats with subtotal renal ablation [15].
• Lupus-like kidney disease in mice deficient in the Src family tyrosine kinases Lyn and Fyn [16].

Biological context of Kidney Diseases

• MRL-lpr mice develop aggressive autoimmune kidney disease associated with increased or de novo renal expression of major histocompatibility complex (MHC) class II molecules and a massive systemic expansion of CD4-CD- double negative (DN) T cells [17].
• Advanced glycation endproducts (AGE) contribute to kidney disease due to diabetes or aging by means of mesangial cell (MC) receptors, such as the receptor for AGE (RAGE), which promote oxidant-stress-dependent NF-kappaB activation and inflammatory gene expression [18].
• The genetic data, bilateral nature of the observed kidney disease, and extent of involvement of the spleen and kidney indicate that, in affected animals, loss of the wild-type Tsc2 allele occurred during embryogenesis, probably as a result of chromosome nondisjunction, with affected animals being mosaics for loss of Tsc2 gene function [19].
• Renal insulin resistance syndrome, adiponectin and cardiovascular events in patients with kidney disease: the mild and moderate kidney disease study [20].
• Previous studies have demonstrated that inhibition of thromboxane A2-dependent platelet aggregation by the thromboxane A2 synthase inhibitor, OKY 1581, ameliorated the progressive kidney disease of rats with subtotal renal ablation [21].

Anatomical context of Kidney Diseases

• Expansion of the glomerular mesangial matrix (MM), thickening of the glomerular basement membrane (GBM), and eventually the development of glomerulosclerosis are often seen in immunologically mediated kidney diseases [22].
• Erythrocyte PAF-acetylhydrolase activity in various stages of chronic kidney disease: effect of long-term therapy with erythropoietin [23].
• Further, the therapeutic value of retinoids in animal models of kidney diseases, such as lupus nephritis, puromycin aminonucleoside nephrosis, anti-glomerular basement membrane nephritis, mesangioproliferative nephritis, and acute renal allograft rejection has been unveiled recently [24].
• Progression of kidney disease: blocking leukocyte recruitment with chemokine receptor CCR1 antagonists [25].
• These results suggest that M-CSF production within the kidney, particularly by tubular epithelial cells, plays an important role in regulating local macrophage proliferation in experimental kidney disease [26].

Gene context of Kidney Diseases

• Autosomal-dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and is characterized by progressive cyst formation and ultimate loss of renal function [27].
• VavP-Bcl2 mice also had a propensity to develop kidney disease of the autoimmune type [28].
• Screening of these mutations may facilitate epidemiologic studies of C4 in infectious, autoimmune, and kidney diseases [29].
• Complete complement components C4A and C4B deficiencies in human kidney diseases and systemic lupus erythematosus [29].
• In contrast, Stat6-deficient NZM mice display a significant reduction in incidence of kidney disease, with a dramatic increase in survival, despite the presence of high levels of anti-dsDNA Abs [30].

Analytical, diagnostic and therapeutic context of Kidney Diseases

• Among chronic kidney disease patients with epoetin-associated PRCA, epoetin discontinuation and immunosuppressive therapy or renal transplantation is necessary for hematologic recovery [31].
• In addition, Pax-2 mouse mutants provide an animal model for human hereditary kidney diseases [32].
• Progression of kidney disease was defined as doubling of baseline serum creatinine and/or terminal renal failure necessitating renal replacement therapy [33].
• Renal dysfunction was defined as an increase in serum creatinine of at least 0.4 mg/dl or a death or hospitalization as a result of chronic kidney disease between the second (1990 to 1992) and fourth (1996 to 1998) examinations [34].
• CONCLUSIONS: The pharmacokinetic and pharmacodynamic profiles and safety data for darbepoetin alfa demonstrate that it can be administered less frequently than epoetin in patients with chronic kidney disease receiving hemodialysis, thus simplifying anemia management [35].

References