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Biomedical subjects

R Nowack

Publications and source records attributed to R Nowack.

12 recordsLinked to original sources
PubMed1992

Subacute effects of thiazide administration on renal hemodynamics and calcium metabolism.

To elucidate the renal effects of thiazides as a function of sodium intake, 8 healthy volunteers without renal disease were studied at baseline and 1 day as well as 4 days after the administration of 100 mg hydrochlorothiazide/day. The subjects were compared on two different dietary sodium intakes (120 mmol/day and 220 mmol/day). Measurements comprised inulin clearance (Cin) and paraaminohippurate clearance (Cpah) by infusion clearance technique, total and ionised calcium, immunoreactive parathyroid hormone (1.84 iPTH), 1.25 (OH)2 vitamin D3, and indices of hemoconcentration. Acute administration of hydrochlorothiazide (HCTZ) caused no change in Cin (before 111 +/- 3 ml/min 1.73 m2; 24 h after, 107 +/- 2 ml/min 1.73 m2) or Cpah (before, 579 +/- 9 ml/min 1.73 m2; after, 584 +/- 12 ml/min 1.73 m2), while a significant (P less than 0.01) decrease was noted on the 4th day after 100 mg HCTZ/day and normal sodium intake. No significant change of creatinine clearance (Ccr) was seen with either manouever. Renal hemodynamic changes after HCTZ administration were marginal when hemoconcentration was prevented by a high salt intake. Acute administration (1 h) of HCTZ caused suppression of 1.84 iPTH (before, 2.3 +/- 0.5 pmol/l; after, 1.9 +/- 0.2 pmol/l; P less than 0.01), but after 4 days a lower ionised calcium (baseline, 1.25 +/- 0.01 mmol/l; day 5, 1.20 +/- 0.02 mmol/l; P less than 0.01) was noticed in parallel with hemoconcentration, metabolic alkalosis, and reduced 1.25 (OH)2 vitamin D3 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Lead intoxication--new insights into an old problem.

The epidemiology, clinical symptomatology, diagnosis and management of acute and chronic lead intoxication are reviewed. While acute lead intoxication has become rare, the elevated environmental lead burden is thought to play a causal role in hypertension. Lead may also be linked with neuropsychological disorders of children and possibly even chronic renal failure. The epidemiological and experimental evidence for this hypothesis is critically discussed.

Adolescent↗
PubMed1992

Renal hemodynamics in recent-onset type II diabetes.

Glomerular hyperfiltration is thought to play an important role in the genesis of diabetic nephropathy. While hyperfiltration is well documented in early type I diabetes, the evidence for hyperfiltration in type II diabetes is conflicting. We investigated 16 nonproteinuric patients with recently diagnosed type II diabetes. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured as inulin clearance (CIN) and p-aminohippuric acid clearance (CPAH) using a constant infusion technique. Lean body mass was measured by densitometry (weighing under water). Renal hemodynamics were also measured in 31 healthy volunteers and six obese nondiabetic individuals. Median GFR in diabetics (133 mL/min/1.73 m2; range, 95 to 165) was significantly (P < 0.01) higher than in obese nondiabetic controls (median, 118; range, 95 to 139). Elevated GFR (ie, > 95th percentile of nonobese healthy controls) was found in 44% of patients. When GFR was factored for lean body mass, it was elevated in 50%. GFR did not correlate with fasting glucose, hemoglobin A1C (HbA1C), insulin-like growth factors, IGF-1 and IGF-2, or somatomedin-binding protein (SMBP). The findings document that hyperfiltration is common in recent-onset type II diabetics.

Adult↗
PubMed1992

The response of GFR to amino acids differs between autosomal dominant polycystic kidney disease (ADPKD) and glomerular disease.

We compared the glomerular filtration rate (GFR) response to amino acids in patients with glomerular disease and polycystic kidney disease. The GFR response to infusion of amino acids (75 g/12 h), of dopamine (2 micrograms/kg per min), or their combination was evaluated in nine healthy probands and in patients with two types of renal diseases at various degrees of renal function: 15 patients with ADPKD and 11 patients with glomerular disease (IgA glomerulonephritis or diabetic nephropathy). Steady-state inulin infusion technique was used. In healthy subjects amino acids increased median C(in) in response to amino acids was not found in glomerular disease. In contrast in most ADPKD patients median C(in) increased after amino acids (+6.0 ml/min; range -4 to +68), (P less than 0.05). The response to amino acids was not modified by dopamine. The results demonstrate that amino acid-induced acute changes of glomerular filtration differ in polycystic kidney disease compared with glomerular disease. These observations may have implications with respect to mechanisms of progression.

Adult↗
PubMed1991

Preservation of renal function in diabetic patients.

Hypertension in type I diabetes appears to be causally related to nephropathy, whereas the relationship between hypertension and type II diabetes is more complex, hypertension being present in the absence of clinically overt nephropathy and even preceding the onset of diabetes. In the diabetic, hypertension is exquisitely sodium-sensitive. It is in diabetic nephropathy that the best evidence has been obtained that treatment of hypertension retards the progression of renal failure. Consensus is still lacking with respect to the point when antihypertensive treatment should be started and the target blood pressure that should be aimed at. Currently, there is no evidence in humans that converting enzyme inhibitors are superior to alternative antihypertensive agents in retarding progression, but tantalizing preliminary evidence on this has been reported in nondiabetic patients with renal failure.

Animals↗
PubMed1991

[Renal effects of conversion enzyme inhibitors].

Recently it has been recognized that even minor elevations of blood pressure contribute to progression of renal failure. Furthermore it has been documented that antihypertensive treatment retards progression of renal failure. Despite impressive experimental data firm clinical evidence, incontrovertible on biostatistical grounds, is not yet available to document that converting enzyme inhibitors (CEI) are superior to alternative antihypertensive agents with respect to halting progression. CEI undoubtedly reduce albuminuria, independent of their effect on systemic blood pressure, and this is related to alterations of glomerular permeability. Recent experimental data suggest that growth processes in damaged kidneys are an important aspect of progression. It is a fascinating perspective, but yet unproven, that CEI interfere with these processes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Detrimental and beneficial effects of converting enzyme inhibitors on the kidney.

It has been recognized recently that even minor elevations in blood pressure contribute to progression of renal failure and that antihypertensive treatment retards progression. Despite suggestive experimental data, no unequivocal clinical evidence is available to date to document that converting enzyme inhibitors (CEIs) are superior to alternative antihypertensive agents with respect to halting progression. CEIs undoubtedly reduce albuminuria, independent of their effect on systemic blood pressure, and this is related to alteration of glomerular permselectivity. Recent experimental data suggest that growth processes in damaged kidneys are an important aspect of progression. It is a fascinating perspective, but yet unproven, that CEIs interfere with these processes.

Angiotensin-Converting Enzyme Inhibitors↗