[Diagnostic criteria of analgesic nephropathy in hemodialyzed patients with chronic renal failure].
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Biomedical subjects
Publications and source records attributed to F Kokot.
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Thorough studies of kidney specimens obtained at autopsy or by renal biopsy revealed, that in noninflammatory acute renal failure oliguria/anuria is caused by increased activation o the renal renin-angiotensin system and increased generation of adenosine. At the polyuric phase moderately increased adenosine in kidney tissue seems to be the main factor responsible for decreased glomerular filtration.
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In 9 clinics 177 patients (68 men and 109 women) aged 23-69 years with primary hypercholesterolemia (TC above 6.5 mmol/L) were treated with lovastatin for 12 weeks. The treatment was started with 20 mg daily. The dose was doubled every 4 weeks, if the total serum cholesterol level did not fall below 5.2 mmol/L. For 4 weeks before treatment with lovastatin all patients received placebo. After the first 4 weeks of therapy the mean TC level decreased significantly (from 8.09 mmol/L to 6.54 mmol/L) by 18.5%. In comparison with the results after placebo (the starting value), after the 8 weeks of the therapy the TC level reduction reached 22.4% and after 12 weeks 23.5%. The mean LDL cholesterol decreased by 26.1%, 30.8% and 32.9% after 4.8 and 12 weeks of lovastatin treatment respectively. An increase in HDL cholesterol by 5.9%, 6.0% and 7.6% and decrease in triglyceride level by 10.7%, 14.9% and 14.0% respectively was also observed. In 6 patients on lovastatin treatment symptoms of acute pancreatitis in 1 case, a cataract in 1 case and aggravation of coronary insufficiency in 4 cases were noticed. These symptoms in the light of our knowledge of the mechanism of action of the drug used and of its side effects described in other trials, may be considered of independent on lovastatin. The treatment was discontinued in 5 cases (because of gastrointestinal intolerance in 2 patients, of aggravation of coronary insufficiency in 2 patients and of pain in the right hypochondrium in 1 patient who himself decided to stop the therapy).(ABSTRACT TRUNCATED AT 250 WORDS)
This paper aimed to assess the influence of opioid receptors on plasma level of atrial natriuretic peptide (ANP) in 12 kidney transplant patients (KTP) with stable graft function and in 15 healthy subjects (control). In KTP significantly higher plasma levels of ANP were found under basal conditions than in control subjects. After blockade of opioid receptors by naloxone a significant decline of plasma ANP was noticed, which was significantly more marked in KTP than in normals. Data obtained in this study suggest, that opioid receptors do influence plasma ANP levels both in KTP and healthy subjects. This influence seems to be significantly more marked in KTP than in normals. Hyperendorphinism seems to be involved in the pathogenesis of elevated plasma ANP levels in KTP.
As already reported short-term rHuEpo treatment influences plasma insulin, glucagon, pancreatic polypeptide (PP), and gastrin secretion in haemodialysed patients. The present study aimed to assess the influence of long-term rHuEpo treatment on secretion of above mentioned hormones. A total of 27 haemodialysed patients and nine healthy subjects were examined. Nine patients with uraemic anaemia were treated with rHuEpo for 12 months (Epo group) while another nine patients did not receive rHuEpo (non-Epo group), but were monitored biochemically and clinically as patients of the Epo group. The third group (HD) comprised nine haemodialysed patients with a haematocrit value of > or = 30% without rHuEpo therapy. In all subjects plasma levels of insulin, glucagon, gastrin, and PP were estimated before and after administration of a test meal. Patients of the Epo group were examined before and after 6 and 12 months of rHuEpo treatment (patients of the Epo group) or clinical monitoring (patients of the non-Epo group) respectively, while only one test was performed in patients of the HD group and healthy subjects. Six months of rHuEpo treatment was followed by an increase of fasting insulinaemia and a decrease of basal plasma level of glucagon and PP. At that time point rHuEpo therapy also increased the response of insulin, glucagon, and gastrin to the test meal.(ABSTRACT TRUNCATED AT 250 WORDS)
Exacerbation of secondary hyperparathyroidism (as manifested by calcium deposits and local inflammation in periarticular tissues) has been reported in haemodialyzed (HD) uraemic patients treated with recombinant human erythropoietin. However, short-term treatment with recombinant human erythropoietin (r-Hu EPO) did not influence significantly plasma levels of parathyroid hormone (PTH), calcitonin (CT) and 25-hydroxycholecalciferol (25-OHD3) in uraemic HD patients. The present study aimed to assess the effect of long-term r-Hu EPO therapy for 12 months on plasma PTH, CT, 25-OHD3 and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) in uraemic HD patients.
PTH is incriminated as an uraemic toxin involved in the pathogenesis of anaemia in chronic renal failure. This fact was the background of our present studies performed in 14 patients with noninflammatory acute renal failure (NARF). Plasma levels of erythropoietin (EPO) and parathyroid hormone (PTH) were estimated in the anuric/oliguric (a/o) and polyuric (p) phase of NARF. In the a/o phase plasma EPO levels were predominantly normal, although inappropriately low to the degree of anaemia. In 50% of patients with NARF episodic short-term increases of plasma EPO levels were noticed which were not caused by worsening of anaemia. In the p phase plasma EPO concentrations were in the normal range (17.9 +/- 3.3 mU/ml) in spite of the same degree of anaemia as in the a/o phase. Plasma PTH levels were significantly elevated during the a/o phase (1.14 +/- 0.1 ng/ml), with a tendency to decline in the p phase (0.87 +/- 0.2 ng/ml). No correlation was found between plasma EPO and PTH concentrations. Results presented in this study suggest presence of relative EPO deficiency both during the a/o and p phases of NARF. As plasma PTH levels were not significantly correlated with serum EPO concentrations, its role in the pathogenesis of suppressed EPO levels seems unproven. Results presented in this study suggest deterioration of the physiological feedback between EPO secretion and the magnitude of erythropoiesis in NARF.
Recent studies suggest the existence of a relationship between the renin-angiotensin system and erythropoietin (EPO) secretion. It has been studied whether patients with various forms of arterial hypertension (essential, renal, renovascular, in the course of arteritis) differ with respect to EPO secretion and whether EPO serum levels are related to renin response induced by dietary sodium restriction to 10-20 mmol Na/24 h for 3 days and upright body position for 3 h. Patients with different forms of hypertension and normal renal excretory function and healthy subjects did not differ in hematocrit value, markers of iron metabolism, and EPO secretion except for patients with arteritis who had higher ferritin values. In these patients a positive correlation between EPO levels and hematocrit values suggests the existence of an altered regulation of EPO secretion. In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production.
Urinary excretion of calcium, magnesium, phosphate and oxalate in the condition of low-calcium diet, and the secretion of LH, FSH, testosterone and estradiol following LH-RH stimulation test have been determined in 26 men with active nephrolithiasis and in 14 healthy male subjects. Significantly higher urinary excretion of calcium and oxalate, and significantly lower excretion of magnesium was observed in men with nephrolithiasis as compared to healthy men. In addition, the patients with nephrolithiasis had significantly higher concentrations of testosterone, estradiol and FSH than the healthy controls. The results obtained suggest the participation of the gonadal hormones in the pathogenesis of active nephrolithiasis.
UNLABELLED: Relationship was assessed between the type of renal pathology and the degree of plasma protein and lipid abnormalities in 59 patients with nephrotic syndrome due to chronic glomerulonephritis (GN). All patients were divided into 5 subgroups according to the type of renal pathology (extracapillary proliferative GN--23, mesangioproliferative GN--18, membranous GN--5, minimal changes--5, other--8 patients) and according to the presence (22 patients) or absence (37 patients) of altered interstitium (inflammation and/or fibrosis). In all patients the following parameters were analyzed: plasma levels of creatinine, total cholesterol and lipids, triglycerides, total protein, electrophoretic fractions of plasma proteins and urinary protein excretion. Type of renal pathology as well as presence of interstitial lesion did not influence the degree of protein and lipid abnormalities in nephrotic patients. Significantly more marked (p < 0.05) abnormalities in the serum and lipid profile were found in patients in whom 76-100% of all glomeruli were abnormal than in patients with a lower percentage of damaged glomeruli. CONCLUSION: Percentage of damaged glomeruli but not the type of renal pathology (glomerular or/and interstitial) are the main factors influencing the magnitude of abnormal serum protein and lipid profiles in nephrotic patients.
The present study aimed to answer the following questions: 1. do secretion of volume related hormones in patients with EH pre and post treatment with captopril differ from normotensive subjects if examined in thermal dehydration conditions; 2. is the electrolyte composition of thermal sweat related to the plasma profile of volume related hormones? and 3. does treatment by captopril influence sweat electrolytes in EH patients. In 16 patients with EH and in 20 healthy subjects a thermal dehydration test was performed. In patients with EH this test was done twice: before treatment and after 6 weeks of captopril therapy. In all subjects plasma renin activity (PRA), aldosterone (Ald) AVP and ANP were measured before and after thermal dehydration. In sweat samples collected after 15' and 45' of thermal dehydration the concentration of Na, K and Cl was assessed. In hypertensive patients before captopril treatment significantly higher values of PRA, ALD and ANP were found, while sweat concentrations of Na and Cl were significantly lower than in controls. After captopril treatment sweat electrolytes concentrations showed a tendency to normalize. No significant correlation was found between the plasma hormonal profile and sweat Na, K and Cl concentrations respectively both in controls and patients with EH pretreatment. A significant positive correlation was noticed only in hypertensive patients post-treatment between plasma aldosterone and sweat Na and Cl concentration respectively. Results obtained in this study show, that volume related hormones (Ald, AVP, ANP) do not seem to influence markedly the electrolyte composition of thermal sweat both in healthy subjects and in hypertensive patients.
In 16 hypertensive patients with significant unilateral renal artery stenosis plasma renin activity (PRA) and plasma levels of adrenaline (A), noradrenaline (NA) and dopamine were assessed in arterial blood, renal venous blood of the ischemic (IK) and normally (NK) perfused kidney and in blood withdrawn from the inferior vena cava, distally from the orifices of the renal veins. Plasma levels of A (= 661.8 +/- 187.7 pg/ml) and NA (= 396.3 +/- 72.5 pg/ml) in renal venous blood of the ischemic kidney were significantly greater than in renal venous blood of the normally perfused kidney (A = 123.4 +/- 16.0 pg/ml; NA = 277.2 +/- 55.6 pg/ml) and than in arterial blood (A = 68.44 +/- 8.4 pg/ml; NA = 192.8 +/- 28.9 pg/ml) and inferior vena cava blood (A = 67.8 +/- 7.5 pg/ml; NA = 182.6 +/- 26.8 pg/ml). In contrast to A and NA, plasma D level in renal venous blood of the normally perfused kidney was significantly higher (= 27.9 +/- 4.9 pg/ml) than in renal venous blood of the ischemic kidney (= 14.3 +/- 2.1 pg/ml) and than in arterial blood (= 16.1 +/- 1.9 pg/ml) and in blood of the inferior vena cava (= 16.3 +/- 1.8 pg/ml). A significant positive correlation was found between PRA and plasma levels of A and NA respectively only in renal venous blood of the ischemic kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: Acute rejection is characterized by renal ischaemia which in turn is a triggering factor of EPO synthesis. On the other side during acute rejection (AR) the plasma PTH level (which is incriminated as an uraemic toxin) increases. This facts justified our present study which aimed to assess: 1. the influence of acute graft rejection (AR) on plasma EPO and PTH levels in KTP and 2. the influence of kind of antirejection therapy i.e. high dose of methylprednisolone (MP) vs thymoglobuline (TG) + moderate dose of methylprednisolone on plasma EPO and PTH levels respectively. A total of 28 KTP were studied who were divided into two groups: the first one designed as group MP comprised 17 KTP treated by high doses of MP while the second one designed as group ATG--consisted of 11 KTP treated by thymoglobulin+moderate doses of MP. The control group consisted of 16 healthy subjects. Before AR KTP showed inappropriately reduced EPO plasma levels when related to the degree of anaemia. AR was accompanied by a significant increase of plasma EPO and PTH levels in all examined KTP groups. After subsidence of AR normalization of plasma EPO and a significant decline of plasma PTH was noticed. A significant positive correlation was found between plasma EPO and PTH levels before the AR period in both examined groups. CONCLUSIONS: 1. KTP are characterized by relative EPO deficiency at the immediate (2-3 weeks) post transplantation period. 2. AR episodes are characterized by a significant rise of both plasma EPO and PTH levels. 3. Changes in plasma EPO and PTH do not seem to be interrelated at the AR episodes.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: 19 patients with active nephrolithiasis, 14 patients with non-active nephrolithiasis and 17 healthy subjects were examined. After 7 days consumption of standardized low calcium, low phosphate, low purine and low protein diet, plasma parathyroid hormone (PTH) and osteocalcin concentration, activity of the alkaline phosphatase and its bone fraction were assessed before and after 4 hours i.v. infusion of calcium gluconate (15 mg/kg b.w. in 500 ml 0.9% NaCl). In addition, urinary excretion of oxalate, calcium, phosphate and magnesium were estimated in all examined groups. CONCLUSIONS: 1. In comparison to healthy subjects, patients with nephrolithiasis are characterized by higher plasma PTH and osteocalcin concentration, increased activity of bone fraction of alkaline phosphatase and urinary oxalate and calcium excretion. 2. Disturbances of calcium-phosphate and oxalate metabolism, PTH secretion and bone osteoblastic activity found in patients with active nephrolithiasis are qualitatively similar but quantitatively more intensive than in patients with non-active nephrolithiasis.
Regulation of renal erythropoietin (EPO) production has not yet been clearly established in physiologic as well as in pathologic conditions. Recent studies suggest a possible role for renin-angiotensin system in control of EPO production. An elevation in blood pressure occurs commonly in patients with various forms of anaemia treated with recombinant human EPO. Furthermore it has been found that EPO can alter secretion of hormones engaged in regulation of intravascular fluid volume and vascular resistance. The aim of this study was to determine whether patients with essential hypertension (EH) and healthy subjects differ in EPO secretion and whether EPO serum level is related to renin response to dietary sodium restriction and upright position of the body. 63 patients with EH and 12 healthy subjects were investigated. Patients with EH were divided into subgroups on the following criteria: renin response to dietary sodium restriction and upright position of the body. 63 patients with EH and 12 healthy subjects were investigated. Patients with EH were divided into subgroups on the following criteria: renin response to dietary sodium restriction and upright position of the body and severity of existing hypertension. In all subjects haematocrit value, haemoglobin concentration, erythrocyte count, sodium, potassium, creatinine, iron, ferritin serum levels, total iron binding capacity, plasma renin activity (PRA), erythropoietin serum level and mean arterial blood pressure (MAP) were measured in basic conditions (normal sodium diet). Additionally PRA, EPO and MAP were measured after dietary sodium restriction for three days and upright position of the body for three hours.(ABSTRACT TRUNCATED AT 250 WORDS)
Secretion of insulin, glucagon, gastrin and pancreatic polypeptide (PP) at basal and test meal stimulation conditions were investigated in 17 patients with essential hypertension (EH) before and after 12 months of treatment with prazosin and in 10 healthy subjects. Before prazosin therapy, patients with EH differ from healthy subject higher insulin and gastrin but lower PP secretion after test meal stimulation. 12 month therapy with prazosin enhanced insulin and suppressed gastrin secretion stimulated by test meal in comparison to the pretreatment values. Prazosin therapy did not influence significantly glucagon and PP secretion. Our results suggest, that long term prazosin treatment markedly influenced insulin and gastrin secretion in patients with EH.
UNLABELLED: The influence of prazosin treatment for 12 months on basal and LH-RH stimulated FSH, LH, estradiol and testosterone secretion and basal and chlorpromazine stimulated prolactin secretion was estimated in 15 male patients with essential hypertension. Male hypertensive patients were characterized by significantly elevated FSH and reduced testosterone secretion as compared with controls. In contrast, plasma LH, prolactin and estradiol concentrations were similar in both examined groups. After 12 months of prazosin treatment basal and stimulated LH and prolactin secretion significantly decreased while estradiol secretion significantly increased. Prazosin treatment for 12 months did not influence significantly LH and testosterone secretion. CONCLUSIONS: 1. Data presented in this study suggest the presence of abnormal function of the pituitary--gonadal axis in male patients with essential hypertension. 2. Long-term prazosin treatment shows an inhibitory effect on FSH and prolactin secretion but stimulatory one on estrogens secretion in male hypertensive patients.