Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0730345 (
microalbuminuria
)
4,018
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Epidermal growth factor (EGF) may have a modulatory role in renal growth and function. The aim of the present study was to evaluate whether urinary excretion of EGF is altered in psoriatic patients with or without arterial hypertension. The glomerular filtration rate was similar in psoriatics as compared with age- and sex-matched controls, whereas urinary EGF (microgram/g creatinine) was significantly reduced in psoriatics: normotensive subjects, 29.52 +/- 3.51 (psoriatics) versus 44.31 +/- 1.20 (controls, p less than 0.05); hypertensive subjects, 19.67 +/- 3.96 (psoriatics) versus 30.11 +/- 1.52 (controls, p less than 0.05). The urinary EGF excretion was lower in males than in females, save for hypertensive psoriatics. Urinary EGF correlated inversely with age and directly with
urinary kallikrein
excretion. Urinary kallikrein activity was reduced and
microalbuminuria
increased in hypertensive psoriatics. These alterations might suggest that initial deterioration of renal function is present in psoriasis.
...
PMID:Depressed urinary excretion of epidermal growth factor in psoriasis. 179 91
The effects of inhibiting angiotensin converting enzyme with perindopril and aldosterone with spironolactone were tested in hypertensive patients over fifty. Accordingly, 75 patients with mild hypertension aged 50 to 70 were randomly divided into three groups for a double-blind 8 week comparison of the actions of placebo, 4 to 8 mg/day perindopril, and 37.5 to 75 mg/day spironolactone. Side-effects caused one patient to withdraw from placebo and one from spironolactone treatment. Mean blood pressure rose by 2.4 mm Hg after placebo but dropped by 7.4 and 8.6 after perindopril and spironolactone (P less than .01). Placebo, perindopril, and spironolactone did not alter blood glucose or plasma potassium, but induced, respectively, variations of -0.09, 0, and +0.34 mmol/L in cholesterol (P = .04), and -0.02, -0.05, and +0.27 mmol/L in triglycerides (P less than .01). After the three treatments, changes in angiotensin converting enzyme activity averaged -1, -6, and -1 mU/mL (P less than .01), in active renin -2, +18, and +28 pg/mL (P less than .01), and in aldosterone, +15, +8, and +95 pg/mL (P less than .01). Placebo, perindopril, and spironolactone did not alter
microalbuminuria
, but reduced
urinary kallikrein
activity by 0.9, 1.8, and 5.4 mU/mmol creatinine (P = .04). Although short-term administration of spironolactone raised renin and aldosterone markedly and lipids moderately (possibly because of volume contraction), the present results show that perindopril and spironolactone are both safe and effective for treating hypertension at the age of 50 or older.
...
PMID:Are angiotensin converting enzyme inhibition and aldosterone antagonism equivalent in hypertensive patients over fifty? 205 95
The aim of the study was to evaluate the role of
urinary kallikrein
in the regulation of renal hemodynamics and sodium handling in insulin-dependent diabetes mellitus (IDDM), and to test the effect of acutely induced hyperglycemia. Urinary kallikrein excretion was evaluated (1) under basal conditions and after stimulation with i.v. furosemide (0.5 mg x kg(-1)), (2) during glycemic clamp-induced eu- and hyperglycemia (5 and 12 mmol/L) and, (3) during time-controlled euglycemia in 21 short-term IDDM patients without
microalbuminuria
and in 18 weight-, age- and gender-matched healthy controls. Sodium excretion and renal hemodynamics using the clearances of inulin and para-amino-hippuric acid were measured during examinations in both groups. The baseline
urinary kallikrein
excretion during clamp-induced euglycemia was comparable in diabetic and control subjects (10.89+/-5.98 versus 10.38+/-3.73 mUE x min(-1)), whereas it was decreased in the baseline for furosemide (5.77+/-3.22 versus 10.9+/-3.7 mUE x min(-1); p < 0.01) and even after furosemide administration (12.0+/-1.6 versus 21.3+/-2.0 mUE x min(-1); p < 0.01) while the patients were hyperglycemic. During intravenous dextrose-induced hyperglycemia, the
urinary kallikrein
excretion significantly declined in diabetic patients (10.89+/-5.98 versus 5.45+/-0.88 mUE x min(-1); p < 0.01), whereas it did not change in controls (10.38+/-3.73 versus 12.55+/-5.47 mUE x min(-1)). A decrease in the fractional excretion of sodium and an attenuated rise in natriuresis after furosemide administration have been found in diabetic compared to control subjects. There were no significant relationships between kallikrein excretion and (1) renal hemodynamics, which was comparable in both groups, or (2) plasma renin activity, plasma and urine aldosterone and cortisol. We conclude that short-term IDDM without renal hemodynamic alterations is associated with decreased basal and furosemide-stimulated kallikrein excretion, which is directly related to the blood glucose level. The decreased activity of the
renal kallikrein
-kinin system might be involved in the increased tendency to sodium retention in diabetic patients.
...
PMID:Decreased urinary kallikrein with hyperglycemia in patients with short-term insulin-dependent diabetes mellitus. 974 43
The aim of this study was to determine the influence of metabolic control of diabetes on natriuresis, the effect of natriuretic peptides and
renal kallikrein
on the kidney and the participation of proximal and distal tubules in natriuresis. The study was done in 41 individuals: 27 IDDM patients and 14 healthy controls. The patients were on insulin only, had normal blood pressure, and were prescribed a standard diabetic diet without sodium or protein restriction. Diabetic patients were assigned to subgroups, depending on the stage of nephropathy and level of metabolic control. Urine collection was done three times daily in all participants. The first collection was done after 500 mg lithium carbonate (p.o.) and was followed by 10 mg amilorid (Midamor, Thomas Morson Pharmaceuticals). The third collection of urine was used to evaluate excretion of cGMP. In addition to sodium, lithium, potassium and creatinine clearances, excretion of
renal kallikrein
, and levels of
microalbuminuria
, fructosamine and glycated hemoglobin were also determined. Lithium clearance was used to evaluate tubular sodium transport. The influence of diuretic peptides--ANP and urodilatin, on natriuresis was reflected by urinary cGMP excretion. Function of the kallikrein-kinin system was studied on the basis of excretion of kallikrein. Amilorid was used to test the effect of blocking amiloride-sensitive sodium channels in distal tubules on natriuresis (Tab. 1). A statistically significant decrease in mean lithium clearance was observed in IDDM patients as compared to healthy controls. Creatinine clearance was the same in both groups (Tab. 2). Lower lithium clearance was observed in the subgroup of diabetic patients with "silent" nephropathy. Diabetic patients with "silent" and early nephropathy had significantly higher levels of fractional sodium reabsorption in the proximal tubule when compared with controls (Tab. 3). Moreover, lower daily excretion of kallikrein was observed in patients with stage II nephropathy in comparison to the control group (Tab. 4). Amilorid uptake had no influence on
urinary kallikrein
. However, natriuresis after amilorid was significantly higher in diabetic patients than in controls. In conclusion, reabsorption in the proximal tubule is increased in patients with "silent" diabetic nephropathy, as revealed by decreased lithium clearance and unchanged creatinine clearance. Hyperactivity of the proximal tubule in stage II and III of diabetic nephropathy results in increased sodium reabsorption in the proximal tubule, as reflected by the increase in fractional sodium reabsorption in this tubule. Amilorid, a distal tubule blocker, reduces distal tubule activity independently of
urinary kallikrein
excretion. Elevated natriuresis was observed after amilorid without any change in
urinary kallikrein
excretion.
...
PMID:[Regulation of natriuresis in diabetic nephropathy]. 1171 8