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Biomedical subjects

A Körner

Publications and source records attributed to A Körner.

16 recordsLinked to original sources
PubMed1992

Sorbinil does not prevent hyperfiltration, elevated ultrafiltration pressure and albuminuria in streptozotocin-diabetic rats.

The effects of aldose reductase inhibition on kidney function were studied in rats with streptozotocin-induced diabetes mellitus. Diabetic rats were fed sorbinil (20 and 50 mg/kg) by daily gastric gavage and were compared with untreated diabetic rats and normal rats. The rats were under daily supervision with regard to blood glucose control, insulin administration and body weight. The aim was to promote continuous body growth and to maintain the blood glucose concentration at around 22 mmol/l without large day-to-day fluctuations. The renal functional changes observed in this well-established diabetic model closely resembled those reported in human Type 1 (insulin-dependent) diabetes mellitus. Sorbinil treatment completely prevented renal cortical sorbital accumulation, but did not abolish kidney enlargement or the increase in ultrafiltration pressure and glomerular filtration rate. Albumin excretion was increased to the same extent in the sorbinil-treated and in the untreated diabetic rats. We conclude that increased metabolism of glucose to sorbitol does not cause the hyperfiltration in rats with streptozotocin-induced diabetes.

Albuminuria↗
PubMed1992

The role of sympathetic-adrenergic activity in the regulation of acid-base homeostasis and renal sodium excretion under acute physical stress in type-I diabetic children (IDDM).

To evaluate the ability of stress response, plasma and urinary catecholamine concentrations, urinary electrolytes and acid-base status were measured in IDDM children (Group I: newly diagnoses 2-4 weeks, n = 7; Group II: duration 5-7 yr, n = 9; Group III: duration 10-13 yr, n = 12). The data were compared to healthy controls, n = 7, (mean +/- SD). Physical stress was induced by 2 W/kg/10 min bicycle ergometer. IDDM children exhibited metabolic acidosis under stress (pH: Group I = 7.24 +/- 0.08; Group II = 7.25 +/- 0.05; Group III = 7.19 +/- 0.03 vs C = 7.36 +/- 0.02). Stress induced an increase in the concentration of plasma norepinephrine (PNE in each group, the most pronounced elevation was seen in Group I (19.36 +/- 8.8 nmol/I vs C = 8.3 +/- 3.2, p < 0.2). Baseline PNE level showed a significant decrease with the duration of IDDM. Excretion of urinary NE (UNE) also increased under stress, however, the highest levels were measured in Group III (580 +/- 209 pmol/min/l. 73m2 vs 290 +/- 124 in Group I, p < .01). Baseline urinary dopamine (UDA) excretions were similar in each group. Stress caused an elevation in UDA only in C (2.05 +/- 1.8 vs 4.59 +/- 2.9 pmol/min.l. 73m2). The ratio of baseline UNE/UDA was similar in Groups I, II and C, but higher in Group III. Stress induced a shift towards NE excretion only in diabetic children which was most pronounced in children having IDDM more than 10 years. Stress did not affect urine output in Groups I. and II., but a decrease was observed in Group III (1.1 +/- 0.3 vs 0.7 +/- 0.3 ml/min.1.73 m2, p < .007). Urinary sodium excretion also decreased in Group III after physical loading (130 +/- 47 vs 66 +/- 33 umol/min/1.73 m2). The data show, that physical stress induces a severe lactic acidosis in IDDM. In spite of the decreased systemic sympathetic activity, the renal catecholamine response showed a shift towards vasoconstriction, sodium and fluid retention under physical stress in IDDM. These changes correlate with the duration of the underlying disease.

Acid-Base Equilibrium↗
PubMed1991

Changes in plasma and urinary amino acid levels during diabetic ketoacidosis in children.

Plasma and urinary concentrations of different amino acids were investigated during diabetic ketoacidosis (DKA) and 12, 24, 72 hours after initiation of therapy. In DKA, plasma concentration of glutamic acid, aspartic acid, valine, leucine and isoleucine significantly increased while that of asparagine and glutamine decreased compared to levels in well-controlled diabetic patients. The urinary excretion of branched-chain amino acids, histidine, serine and threonine was elevated while those of glutamic acid, glutamine, glycine and taurine were reduced. Among the different amino acids, histidine excretion had the highest variability. A strong correlation was found between the urinary excretion of several amino acids and that of the beta-2-microglobulin characterizing tubular dysfunction. Changes in the excretion of different amino acids reflect the altered metabolic state and renal function due to DKA.

Adolescent↗
PubMed1991

Renal functional effects of prostaglandin synthesis inhibition in patients with insulin-dependent diabetes mellitus of long duration without nephropathy.

The short-term effects of prostaglandin synthesis inhibition (PGSI; single dose 500 mg of naproxen) on renal function were studied in six women (age: 21.9 +/- 2.4 yrs) with insulin dependent diabetes mellitus (IDDM) of 14.3 +/- 2.8 yrs' duration, and in nine age- and sex-matched controls. The diabetics had no overt signs of nephropathy (Albustix neg, normal serum creatinine, and blood pressure). The clearance of inulin (CIn) and PAH; the filtration fraction (FF); and the excretion of Na, albumin and PGE2 were studied under water diuresis on two separate mornings, first without and then with PGSI. With PGSI all individuals has lower PGE2 excretion. The CIn and FF were significantly (p less than 0.05) higher in the diabetics than in the controls both without (129.4 +/- 23.9 ml/min/1.73 m 2 and 23.4 +/- 2.8% vs. 107.6 +/- 10.3 and 19.7 +/- 1.6) and with (133.7 +/- 29.4 and 22.6 +/- 2.1, vs. 106.8 +/- 10.3 and 20.1 +/- 1.5) PGSI. The diuresis and Na excretion were significantly lower with PGSI, than without, in both groups. The albumin excretion was significantly higher in the diabetics under both conditions (29.9 +/- 16.6 and 34.2 +/- 19.9 micrograms/min/100 ml GFR, vs. 14.5 +/- 10.6 and 12.9 +/- 8.3 in controls). We conclude that the hyperfiltration in this stage of IDDM does not appear to be PG dependent, and that PGSI does not give any immediate effects on the albumin excretion.

Adult↗
PubMed1991

Urinary catecholamine in children with diabetic ketoacidosis.

Urinary excretion of norepinephrine, epinephrine and dopamine was investigated in children with diabetic ketoacidosis. Besides pronounced hyperglycemia and metabolic acidosis, severe hypovolemia was also observed. At the onset of the study, urinary excretion of norepinephrine, epinephrine and dopamine was markedly elevated. Fluid replacement decreased urinary catecholamine excretion. Norepinephrine: 996 +/- 97 vs. 253 +/- 29; dopamine: 5,108 +/- 480 vs. 3,175 +/- 715; epinephrine: 402 +/- 81 vs. 77 +/- 200 pmol/min/1.73 m2. During ketoacidosis, there was a significant negative correlation between urinary norepinephrine excretion and endogenous creatinine clearance. Urinary output of both norepinephrine and dopamine correlated significantly with diuresis, while sodium excretion only correlated with dopamine excretion. Our data suggest that in diabetic ketoacidosis increased urinary excretion of norepinephrine may participate in renal hypoperfusion and hypofiltration. Elevated renal dopamine production contributes to sodium loss, characteristic for diabetic ketoacidosis.

Adolescent↗
PubMed1990

[Follow-up of blood and urinary amino acid concentrations in diabetic ketoacidosis in children].

Plasma and urinary concentrations of amino acids were investigated during diabetic ketoacidosis (DKA) and 12, 24, 72 hours after initiation of therapy. In DKA plasma concentration of glutamic acid, asparaginic acid, valine, leucine and isoleucine significantly increased while that of asparagine and glutamine decreased compared to levels in well controlled diabetic patients. Despite the elevated urinary excretion of branched chain amino acids, histidine, serine and threonine, urinary excretion and clearance of glutamic acid, glutamine, glycine and taurine were reduced. Among the different amino acids histidine excretion had the highest variability. Strong correlation was found between the urinary excretion of several amino acids and that of the beta-2-microglobulin characterizing tubular dysfunction. Changes in the excretion of different amino acids reflect the altered metabolic state and renal function due to diabetic ketoacidosis.

Adolescent↗
PubMed1990

Urinary prostaglandins in hyperglycaemic ketoacidosis of type I diabetes mellitus.

Urinary excretion of various renal prostaglandins was measured by radioimmunoassay and gas chromatography-mass spectrometry in children who had different degrees of metabolic control. Excretion in PGE2 in diabetic children was twice control values irrespective of the presence or absence of diabetic ketoacidosis (DKA). The urinary excretion of PGF2 alpha was significantly increased in diabetic children with ketoacidosis, but not when diabetes was well controlled. The excretion of 13, 14 dihydro-15-keto PGE2, the major metabolite of circulating PGE2, was increased in all diabetic children, and was most elevated in ketoacidosis when it averaged 10 times basal excretion. Urinary excretion of PGF2 alpha and of 6-keto-PGF1 alpha, the metabolite of PGI2, was approximately doubled in DKA compared with values from healthy subjects. Excretion of PGE2 was twice control values in children with stable diabetes, whereas the equivalent value for TXB2, the metabolite of the active vasoconstrictor TXA2, was reduced by approximately 50%. We suggest that the increased excretion of prostacyclin metabolite may result from a protective biological action on the kidney opposing other vasoconstrictor hormone activity. PGE2 appears not to be involved in this process. The highly elevated excretion of PGE2 metabolite may represent an activation of systemic PGE metabolism during DKA.

Adolescent↗
PubMed1990

Reduced glomerular filtration and elevated urinary protein excretion in diabetic ketoacidosis.

Glomerular filtration rate (GFR) was measured by two methods in 9 children with diabetic ketoacidosis (DKA), directly by true creatinine clearance and indirectly by means of serum beta-2-microglobulin levels. We found significantly reduced GFR in the first hours of DKA. The rapid improvement in GFR after fluid and electrolyte replacement indicates that volume depletion is the major cause of low filtration rate. In spite of the reduced GFR we observed pronounced albuminuria and low molecular weight (LMW) proteinuria. We conclude that the pathological albuminuria and microalbuminuria in DKA are caused not by glomerular hyperfiltration but by tubular dysfunction.

Adolescent↗
PubMed1987

Atrial natriuretic peptide and other vasoactive hormones during treatment of severe diabetic ketoacidosis in children.

Plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), renin activity (PRA), aldosterone, norepinephrine, and cortisol, and renal functions were investigated in nine children with diabetic ketoacidosis. Before therapy, blood glucose concentration was 608.4 +/- 142.2 mg/dL and base excess -21 +/- 1.9 mmol/L. The calculated volume depletion was 2505 +/- 1005 mL/1.73 m2. At the onset of the study, the plasma concentration of ANP (5.3 +/- 1.2 fmol/L) was low, and concentrations of AVP (159 +/- 44 pg/mL), PRA (59 +/- 19 ng angiotensin l/mL/hr), aldosterone (114 +/- 11 ng/dL), norepinephrine (430 +/- 67 pg/mL), and cortisol (33 +/- 2.1 micrograms/dL) were markedly elevated. Fluid replacement raised plasma ANP concentration, which reached physiologic levels on the first day of therapy. PRA, aldosterone, norepinephrine, and cortisol also normalized during the first 24 hours of therapy, whereas AVP remained above the physiologic range at 20.4 +/- 6.8 pg/mL on the third day. Our data indicate that in diabetic ketoacidosis, volume depletion, enhanced sodium excretion, and hyponatremia activated vasoconstrictor and sodium-retaining hormone systems and that secretion of the natriuretic and vasodilator hormone ANP is suppressed. All of these hormonal alterations seem directed at maintaining adequate fluid volume and sodium homeostasis.

Adolescent↗
PubMedDate not supplied

Hyperinsulinuria in diabetic ketoacidosis.

Urinary insulin excretion has been measured in diabetic children. In nine well controlled diabetics urinary insulin excretion (mean and 2SD) was significantly greater than that found in healthy controls (8.8; 4.4-17.5 versus 3.8; 2.3-6.4 microU/min/1.73 m2). In ten ketoacidotic diabetic children a 50 fold increase of the urinary insulin excretion has been observed (464.8; 158.2-1363 microU/min/1.73 m2). The hyperinsulinuria proved to be reversible: significantly decreased excretion rate (12.9; 9.7-12.3) could be measured 8-10 days after recovery from coma. The hyperinsulinuria during ketoacidosis indicates severe reversible tubular dysfunction. Recurrent ketoacidotic episodes might play a role in the development of diabetic nephropathy.

Adolescent↗