CRF can accelerate CAC progression.CRF increases the expression of pro-inflammatory factors, electrolyte imbalance (e.g., of calcium, phosphorus), parathyroid hormone, and uremic toxins and their ability to promote calcification.
ESRD was also associated with a shift in MAIT PMA-induced cytokine production away from IFNγ production and toward granulocyte macrophage-colony stimulating factor (GM-CSF) secretion, and a loss of <i>E. coli</i>-stimulated tumor necrosis factor α expression.
ESRD was also associated with a shift in MAIT PMA-induced cytokine production away from IFNγ production and toward granulocyte macrophage-colony stimulating factor (GM-CSF) secretion, and a loss of <i>E. coli</i>-stimulated tumor necrosis factor α expression.
B1R gene G-->C substitution at position -699 in the promoter region and B2R gene C-->T transition at position 181 in exon 2 were genotyped in 247 family trios: offspring affected with ESRD and both parents.
Renin-angiotensin system is considered important in the genesis of hypertension and development of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD).
Uteroglobin GG genotype may be a genetic marker for rapid disease progression to end-stage renal failure, especially in the IgAN patients with heavy proteinuria or high blood pressure.
Renin-angiotensin system has been implicated in the development of intraglomerular hypertension and has a central role on progression in chronic renal disease.
HNF-1 beta gene mutation screening may prove useful in patients with small cystic kidneys and chronic renal failure, in whom a definite renal diagnosis could otherwise only be established by renal biopsy.
Haptoglobin homozygosity seems to represent a possible risk factor for CRF in hypertensive, diabetic and PKD patients; Hp heterozygosity may lead to chronic glomerulonephritis.