Factor VIII procoagulant activity (VIII-C), related antigen (VIII-AG), and von Willebrand factor (VIII-vWf) were measured in 38 patients with chronic renal failure (CRF), in 19 patients with normal renal function from a general medical ward, and in 17 normal subjects.
In PKD1 families, resemblance in age of onset of ESRD was apparent; variation was less within than between families (F = 13.0, P less than 0.0001), and risk of false negative ultrasonographic diagnosis appears largely restricted to families in which ESRD occurs relatively late.
Mutations in the COL4A5 collagen gene have been implicated as the primary defect in Alport syndrome, a heritable disorder characterized by sensorineural deafness and glomerulonephritis that progresses to end-stage renal failure.
The case we report is a 46,XX phenotypic female child who had diffuse mesangial sclerosis (DMS) and developed Wilms tumor 3 years after initiating dialysis for end-stage renal disease (ESRD).
Regulated expression of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) genes, induced in cultured peripheral blood mononuclear cells from patients with end-stage renal disease on hemodialysis (HD; N = 13) or peritoneal dialysis (PD; N = 13), was compared to that of 32 normal donors.
Regulated expression of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) genes, induced in cultured peripheral blood mononuclear cells from patients with end-stage renal disease on hemodialysis (HD; N = 13) or peritoneal dialysis (PD; N = 13), was compared to that of 32 normal donors.
HLA-A,B,DR antigens of two groups, one of normal individuals (N- = 31) and another of CRF (Chronic Renal Failure) patients (K- = 37), who did not develop anti-HBs protective antibodies after Hepatitis B (HB) vaccination, were compared, respectively, to the HLA antigens of two corresponding control groups (N+ = 52, K+ = 49), who responded to the vaccine.
The results indicate that deletion polymorphism in the ACE gene, particularly the homozygote DD, is a risk factor for progression to chronic renal failure in IgA nephropathy.
The results indicate that deletion polymorphism in the ACE gene, particularly the homozygote DD, is a risk factor for progression to chronic renal failure in IgA nephropathy.
The peripheral red cell count is kept constant by a closely controlled feedback mechanism involving O2 supply, erythropoietin secretion and erythropoiesis; the system may become unbalanced in conditions such as chronic renal disease, chronic inflammation and prematurity.
Animal studies show that the renin-angiotensin system contributes to hypertension, glomerulosclerosis and progressive chronic renal failure in renal disease.
Anemia is an invariable consequence of end-stage renal failure (ESRF) and recombinant erythropoietin has dramatically improved the quality of life of patients with ESRF.
Thus the secretion of IL-10 might be regarded as a compensatory mechanism which controls monokine induction by chronic renal failure and hemodialysis treatment.
In rare cases, the correlation between the POMC peptides is disrupted by a general disorder selectively modifying the metabolism of the different members of the family as in chronic renal failure, or in tumors where POMC processing is abnormal.
The plasma concentration of immunoreactive guanylin in the normal individuals tested was 31.2 +/- 3.0 fmol/ml (mean +/- SE) and that in patients with chronic renal failure who were undergoing hemodialysis 7,924 +/- 2,140 fmol/ml.
Our experiments demonstrated that TNF inhibitory activity in the urine of CRF patients depended partly on the existence of soluble TNF receptors in the urine.
The granulocyte inhibitory protein (GIP), a 23-kDa protein found to be significantly overexpressed in patients with chronic renal failure, increases autocrine transcription and expression of interleukin (IL) 6 and IL-8 in human mesangial cells.