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Biomedical subjects

H Hohage

Publications and source records attributed to H Hohage.

At least 55 records · Page 3Linked to original sources
PubMed1999

Blood pressure control in kidney transplant recipients: influence of immunosuppression.

1. Disturbances of the blood pressure regulation, probably due to dysfunction of the autonomic nervous system, are well known complications in chronic renal failure. Haemodialysis and transplantation have been reported to ameliorate nerve dysfunction. 2. In this study, the function of the blood pressure control was investigated in kidney transplant recipients after longtime haemodialysis treated with ciclosporine A and tacrolimus and compared to healthy individuals. To investigate the influence of immunosuppression, the measurements were performed twice, at low and high whole blood concentrations of ciclosporine and tacrolimus. Besides ciclosporine, tacrolimus, azathioprine and prednisolone no other drugs were used in the group of kidney transplant recipients. 3. Kidney transplant recipients (KTR) treated with ciclosporine showed reduced blood pressure and heart rate responses to the cardiovascular stress tests (head-up tilt and cold pressure test) under basal conditions. Two hours after ciclosporine application, the differences in the responses to cardiovascular stress tests between KTR and controls were significantly more pronounced. 4. Patients with tacrolimus immunosuppression showed a similar blood pressure and heart rate response under basal conditions. Two hours after drug application, the blood pressure response following orthostatism and heart rate response to the cold pressure test were significantly higher in tacrolimus treated patients. 5. Our results indicate, that kidney transplant recipients still express an altered function of the blood pressure control. Furthermore, ciclosporine A and tacrolimus seem to contribute to dysfunction of the blood pressure regulation by their own. Tacrolimus immunosuppression does not seem to offer advantages concerning the function of the blood pressure control as compared to ciclosporine A.

Adult↗
PubMed1999

Acute and persistant effects of smoking on the baroreceptor function.

Recent studies showed that to smoke four cigarettes within one hour impairs baroreflex sensitivity in humans. In the present study, these effects were qualified more precisely from blood pressure and heart rate records by a sequence analysis and by Fourier analysis of Finapres-registrations. The Mayer waves of the heart rate PDS (power density spectrum), partially representing sympathetic activity, increased during smoking (83.7 +/- 1.0 AU to 89.5 +/- 1.1 AU, P < or = 0.05) and decreased after smoking (86 +/- 1.0 AU, P < or = 0.05). They did, however, not reach baseline levels again within 30 min. Probably due to this, mean arterial blood pressure (64.3 +/- 1.3 mmHg vs. 76.9 +/- 1.3 mmHg, P < 0.05) and heart rate (71.8 +/- 1.4 min(-1) vs. 82.9 +/- 1.4 min(-1), P < 0.05) increased unequivocally after smoking. On the other hand, baroreflex sensitivity decreased dramatically from 15.4 +/- 1 to 11.2 +/- 0.6 ms mmHg(-1) (P < 0.05). This finding was associated with an increased heart rate variability after smoking (6 +/- 0.5 min(-1) vs. 9.2 +/- 1 min(-1)) Thus, the present study provides evidence that chronic tobacco (nicotine)-abuse causes pathologic alterations of the baroreflex control. In synergism with other processes like elevated catecholamine blood levels, these alterations may contribute to the higher risk of cardiovascular diseases.

Blood Pressure↗
PubMed1999

Influence of smoking on baroreceptor function: 24 h measurements.

OBJECTIVE: Recent studies showed that smoking four cigarettes per hour impairs baroreflex sensitivity in humans. In this study, baroreceptor function was qualified more precisely by 24 h measurements using the new portable Portapres system, allowing a continuous non-invasive registration of blood pressure curves. METHODS: Twenty-four smoking individuals (12 male/12 female) who smoked more than 10 cigarettes per day for more than 6 years were investigated. Thirty non-smokers (15 male/15 female) served as controls. Data were evaluated separately for the 08:00-22:00 h and 22:00-08:00 h periods. RESULTS: Within one 24 h period, smokers showed a higher blood pressure [female: mean arterial blood pressure (MAP) 85.5 mmHg; male: MAP 93 mmHg] compared to non-smokers (female: MAP 80 mmHg; male: MAP 90 mmHg). During daytime (08:00-22:00 h), this difference reached a level of statistical significance (P< 0.05) in female subjects. Heart rate was significantly higher in smokers (female: 86 bpm; male: 80 bpm) compared to non-smokers (female: 77 bpm; male: 70 bpm) during the 24 h observation period. The number of sequences (seq) in smokers surpassed the number of sequences in non-smokers by about 53 seq/day, which corresponds to a significant difference of 4.5%. At night the sympathetic -systolic blood pressure/-pulse interval (-SBP/-PI) sequences of the smoking group predominated over the -SBP/-PI sequences in the non-smoking group. On the other hand, the parasympathetic +SBP/+PI sequences were significantly less in smokers between 22:00 and 08:00 h. The regressions (i.e. D pulse interval/D SBP [ms/mmHg]), which represent the baroreceptor sensitivity, were clearly smaller in smokers. CONCLUSIONS: The present study provides evidence that chronic tobacco (nicotine) abuse causes pathological alterations of autonomic nervous blood pressure regulation which can be measured under normal living conditions and may be described as sympathovagal dysbalance and decreased baroreceptor sensitivity. Taken together with processes such as elevated catecholamine blood levels, these alterations may explain the higher risk of cardiovascular diseases.

Adult↗
PubMed1999

Zinc protoporphyrin and percentage of hypochromic erythrocytes as markers of functional iron deficiency during therapy with erythropoietin in patients with advanced acquired immunodeficiency syndrome.

BACKGROUND: We assessed zinc protoporphyrin (ZPP) and the percentage of hypochromic erythrocytes in patients with advanced acquired immunodeficiency syndrome (AIDS) treated with recombinant erythropoietin (rhEPO). METHODS: Patients received 150 IU rhEPO subcutaneously every second day for 10 days, and 150 IU rhEPO plus 62.5 mg of intravenous iron every second day for an additional 10 days. RESULTS: Before rhEPO therapy, ZPP was at 64.3 +/- 27.3 micromol/mol heme and the percentage of hypochromic erythrocytes was elevated at 9.7%, indicating mild functional iron deficiency. Ferritin was 1,002 +/- 956 microg/L, with transferrin saturation of 19.1 +/- 9.7%. Under rhEPO alone, ZPP rose to 80.1 +/- 21.6 micromol/mol heme and the percentage of hypochromic red cells rose to 22.9 +/- 4.7%; ferritin fell to 705 +/- 601 microg/L and transferrin saturation fell to 12 +/- 6.3%. When rhEPO was supplemented with iron, ZPP fell to 70.4 +/- 20.5 micromol/mol heme, the percentage of hypochromic red cells fell to 14.7 +/- 3.4%; ferritin was unchanged at 771 +/- 62 microg/L and transferrin saturation rose to 20.5 +/- 5.5%. CONCLUSIONS: In contrast to ferritin and transferrin saturation, ZPP and the percentage of hypochromic erythrocytes effectively detect the functional iron deficiency under rhEPO therapy in advanced AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients with nephrotic syndrome.

The influence of fluvastatin, a liver-selective, competitive inhibitor of the 3-hydroxymethyl-glutaryl-coenzyme A reductase, on the lipoprotein metabolism was investigated in 9 patients with nephrotic syndrome. All patients had biopsy-proven renal disease as cause of their nephrotic syndrome and exhibited severe hyperlipidemia [baseline: serum cholesterol 358 +/- 46 mg/dl (9.3 mmol/l), low-density lipoprotein cholesterol 236 +/- 18 mg/dl (6.1 mmol/l), triglycerides 333 +/- 28 mg/dl (3.8 mmol/l), and lipoprotein Lp(a) 46 +/- 11 mg/dl]. After 1 year of 40 mg of fluvastatin, significant reductions of total cholesterol by 31% to 242 +/- 26 mg/dl (6.3 mmol/l) and low-density lipoprotein cholesterol by 29% to 162 +/- 12 mg/dl (4.2 mmol/l) were observed. Furthermore, triglyceride values were also lowered significantly by 19% to 268 +/- 21 mg/dl (3.1 mmol/l). Lipoprotein Lp(a) and high-density lipoprotein-cholesterol remained unchanged by fluvastatin. These improvements in lipid profile were maintained during the entire follow-up period of 1 year. There were no adverse events, and the slight increase in serum creatinine observed during the study was considered to be due to the primary renal disease. In conclusion, long- term administration of fluvastatin in patients with nephrotic syndrome appears to be an effective and safe treatment of the hyperlipidemia associated with this disorder.

Adult↗
PubMed1999

ACE inhibitor versus beta-blocker for the treatment of hypertension in renal allograft recipients.

Angiotensin-converting enzyme (ACE) inhibitors have been shown to slow the progression of chronic renal failure. However, the value of ACE inhibitors for the treatment of hypertension in renal allograft recipients has not been established. ACE inhibitors dilate the efferent glomerular arteriole, an effect that may aggravate the decrease in glomerular filtration rate resulting from cyclosporine-induced vasoconstriction at the afferent glomerular arteriole. Therefore, the goal of this double-blind, randomized study was to compare the antihypertensive and renal effects of the ACE inhibitor quinapril with those of the beta-blocker atenolol in renal allograft recipients in whom hypertension developed 6 to 12 weeks after transplantation. All patients received cyclosporine as an immunosuppressant and had stable graft function (serum creatinine concentration, <220 micromol/L) at entry into the study. Twenty-nine patients who received quinapril (daily dose titrated between 2.5 and 20 mg) and 30 patients who received atenolol (daily dose titrated between 12.5 and 100 mg) completed the 24-month study. The two groups did not differ in age, sex ratio, height, and weight before entry into the study. Quinapril decreased diastolic blood pressure from 96+/-1 to 84+/-1 mm Hg (average throughout treatment period), and atenolol decreased diastolic blood pressure from 96+/-1 to 83+/-1 mm Hg. The serum creatinine concentration did not change significantly in either group after 24 months (129+/-8 micromol/L at entry and 148+/-19 micromol/L after 24 months in the quinapril group and 131+/-6 micromol/L at entry and 152+/-15 micromol/L after 24 months in the atenolol group; P=NS for both groups). After 24 months, the change in urinary albumin excretion from baseline was -10+/-15 mg/d in the quinapril group and 52+/-32 mg/d in the atenolol group (P=0.03). These results show that quinapril and atenolol are effective antihypertensive drugs when used after renal transplantation. Moreover, compared with atenolol, quinapril has no adverse effects on graft function. The relative reduction in albuminuria observed with quinapril as compared with atenolol could indicate a beneficial effect of quinapril on long-term graft function.

Adolescent↗
PubMed1999

Clearance of iopromide during haemodialysis with high- and low-flux membranes.

PURPOSE: The present clinical trial addressed the clearance of the contrast medium iopromide, a middle-sized molecule, during dialysis with high- and low-flux membranes. MATERIAL AND METHODS: Twenty chronic haemodialysis patients without residual renal function were dialysed either with low-flux haemophan or high-flux polyamide directly after application of the contrast medium. Iodine concentrations were determined by radiofluorescence methods. RESULTS: Plasma concentrations of iodine before dialysis ranged between 1.1 and 3.9 mg/ml. The mean clearance rates for both membranes were comparable (110+/-1.4 ml/min high-flux and 108+/-1.9 ml/min low-flux), the sieving-coefficient was 0.83 for both membranes. After three hours of dialysis, 58% (high-flux) and 62% (low-flux) of iopromide was removed, half time of elimination was reached after 140+/-16 min (high-flux) and 122+/-11 min (low-flux). CONCLUSION: Our results demonstrated that elimination of iopromide is not dependent on the pore size of the membrane during dialysis. Due to higher blood flow rate, we found a higher elimination rate and a reduced half-time of elimination than prior investigations.

Contrast Media↗
PubMed1998

[Hypotension in acyclovir therapy].

A 51 year old man developed Herpes zoster on the right arm (C5/C6) treated subsequently with aciclovir infusions (500 mg, 3/day). Ten months before hospital admission he did have a radical resection of a epi-oro-hypopharyngeal carcinoma (T4/N1/G2, M0; lymphangiosis carcinomatosa) as well as a partial laryngeal resection for a recurrence 3 months later and removal of a cervical lymph node metastasis after two further months. During aciclovir treatment the patient experienced repeated bradycardia with hypotension verifiable with the tilt-table test. The bradycardias could not be further characterized by ECC. Neither sonography nor CT-scans gave an indication for infiltration of the cervical course of the vagus or glossopharyngeal nerves. Serum catecholamines were, however, markedly reduced. After cessation of aciclovir the bradycardias and hypotensive episodes disappeared. A final tilt-table test was unremarkable. A reversible autonomic neuropathy induced by aciclovir seems a possible explanation.

Acyclovir↗
PubMed1998

Effects of extracellular cadmium on renal basolateral organic anion transport.

Heavy metal ions are well-known nephrotoxic agents. Usually, they induce a damage of various renal transport systems. Cd2+, however, has been shown to enhance renal basolateral organic cation transport. Therefore, the effects of Cd2+ on the basolateral p-aminohippuric acid (PAH) uptake of microdissected nonperfused rabbit kidney S2 proximal tubule segments were investigated. Incubation with Cd2+ induced a bell-shaped concentration response curve with a 2-fold increase of the PAH transport at a Cd2+ concentration of 10(-6) M. Since Cd2+ has been described to activate protein kinase C (PKC), the effects of the PKC inhibitor staurosporine were also tested. Staurosporine (10(-8) M) could, however, not reduce the effects of Cd2+. Cd2+ may exert its effects by an as yet unknown mechanism that is different from the PKC-activating mechanism of phorbol esters. A stimulation of the tricarboxylic acid cycle in kidney cells by Cd2+ may, however, increase the delivery of alpha-ketoglutarate. Indeed, incubation of proximal tubules with alpha-ketoglutarate increased PAH transport across the basolateral membrane significantly. Thus, the observed effects of Cd2+ may be due to an enhanced transport of p-aminohippuric acid by stimulation of exchange of PAH with alpha-ketoglutarate. The modulation of renal organic anion transport may be another aspect of Cd2+ nephrotoxicity.

Animals↗
PubMed1998

Serum antibody titers in a systemic lytic therapy with streptokinase.

BACKGROUND: Anaphylactic reactions to streptokinase are rare but potentially life-threatening complications. Gamma E immunoglobulin (IgE) mediated mechanisms, probably due to streptococcal infections, have been implicated. We investigated the value of in vitro laboratory or dermatologic tests in predicting anaphylactic reactions due to streptokinase and the value of antistreptolysin titers (ASL) in predicting the amount of specific IgE (sIgE) and specific gamma G immunoglobulin (sIgG) neutralizing antibodies to streptokinase. METHODS: We measured serum levels of total IgE, streptokinase sIgE and sIgG, and ASL in 16 patients before and 9 and 41 days after streptokinase therapy. Immediately before therapy, intracutaneous testing with 100 IU streptokinase was done. RESULTS: Dermatologic testing did not identify patients prone to allergic reactions. Moreover, not all patients with increased sIgE levels had allergic reactions. These reactions were independent of the dose of streptokinase given. In spite of steroid prophylaxis, allergic reactions occurred in 3 of 16 patients, but none showed life-threatening anaphylaxis. Streptokinase sIgE and sIgG concentrations were closely related to ASL titers. CONCLUSIONS: Plasma levels of sIgG, sIgE, and ASL titers showed a good correlation. We believe ASL titers can be used for the estimation of neutralizing antibodies instead of streptokinase sIgG antibodies. Currently, no laboratory or dermatologic test allows reliable predictions of allergic reactions to streptokinase.

Adult↗
PubMed1998

Effects of diadenosine polyphosphates on the intracellular Ca2+ concentration in endothelial cells.

Diadenosine polyphosphates have differential hemodynamic effects. The role of the endothelium in the vascular effects of these agonists is still unclear. Primary cultures of rat aortal endothelial cells and Ea.hy 926 cells (a continuous endothelial cell line) were used to investigate the effects of Ap3A-Ap6A, adenosine triphosphate (ATP), and for comparison, arginine vasopressin (AVP) and angiotensin II (A II) on the intracellular Ca2+ concentration, [Ca2+]i. Fura-2 was used as Ca2+ indicator. In rat aortal endothelial cells, ATP and Ap4A concentration dependently increased [Ca2+]i with an initial peak followed by an elevated plateau. The half-maximal effects were reached at approximately 7 micromol/l for ATP and at approximately 10 micromol/l for Ap4A. The maximal peak effects at 100 micromol/l were 1,035 +/- 413 nmol/l (n = 3) and 437 +/- 271 nmol/l (n = 8) for ATP and Ap4A, respectively. At 100 micromol/l Ap3A and Ap6A slightly increased [Ca2+]i, while Ap5A had no significant effect. The known endothelial agonists AVP (100 nmol/l) and A II (10 nmol/l) increased [Ca2+]i initially by 1,549 +/- 913 nmol/l (n = 7) and 209 +/- 45 nmol/l (n = 9), respectively. In Ea.hy 926 cells an increase in [Ca2+]i was obtained only with ATP (10 micromol/l) and with Ap4A (100 micromol/l). Ap3A, Ap5A, and Ap6A (each 100 micromol/l) and also AVP (100 nmol/l) and A II (10 nmol/l) had no significant effects in these cells. These results show that a considerable increase in [Ca2+]i in endothelial cells can only be induced by Ap4A among the diadenosine polyphosphates, indicating that the vasoactive effects of only this polyphosphate could at least partly be mediated via Ca2+-dependent mechanisms in endothelial cells, comparable to the known effects of AVP, A II, and ATP. The fact that A II and AVP did not influence [Ca2+]i in Ea.hy 926 cells is probably due to the loss of the respective receptors in this cell line.

Adenosine Triphosphate↗
PubMed1998

Effects of diadenosine polyphosphates on systemic and regional hemodynamics in anesthetized rats.

Diadenosine polyphosphates (Ap4A, Ap5A, Ap6A) induce vasodilatation or vasoconstriction in various isolated vessels and influence central and peripheral hemodynamics. The influence of diadenosine polyphosphates on hemodynamics was studied in anesthetized rats in vivo. Mean arterial blood pressure (MABP) and heart rate (HR) measured in the carotid artery decreased with Ap4A, Ap5A, and Ap6A. Renal blood flow (RBF), femoral blood flow (FBF) and cardiac output (CO) were evaluated by an ultrasonic transit-time method. Renal superficial blood flow (RSBF) was measured by laser Doppler flowmetry. CO, RBF and RSBF were decreased initially by all three diadenosine polyphosphates. FBF was also slightly decreased. Total peripheral (TPR), renal (RVR) and femoral (FVR) vascular resistances were calculated. TPR was transiently increased by the dinucleotides following by a decrease. RVR and, to a lesser extent, FVR were also increased. These data show that diadenosine polyphosphates have effects on both the heart and the peripheral blood vessels. The effects on the heart and MABP were dominated by bradycardia and hypotension. In the kidney, diadenosine polyphosphates induced a predominant vascoconstriction. The effects on skeletal muscle blood flow were much smaller. Thus, the three diadenosine polyphosphates studied differ in the effects on heart and peripheral vessels.

Animals↗
PubMed1998

Regulation of organic cation transport in IHKE-1 and LLC-PK1 cells. Fluorometric studies with 4-(4-dimethylaminostyryl)-N-methylpyridinium.

The regulation of transport of the fluorescent organic cation 4-(4-dimethylaminostyryl)-N-methylpyridinium (ASP+) by renal proximal tubular organic cation transport was studied in IHKE-1 and LLC-PK1 cells with a recently established fluorometric technique (Stachon et al., 1996, 1997). Stimulation of Ca++/diacylglycerol-dependent protein kinase by 1,2-dioctanoyl glycerol (DOG; 0.01-1 mumol/l, n = 7), ATP (0.1 mmol/l, n = 9), oxytocin (0.1 mumol/l, n = 6) and bradykinin (1 mumol/l, n = 7) resulted in an increase of ASP+ accumulation in IHKE-1 cells by 35 +/- 9% (DOG), 65 +/- 30% (ATP), 66 +/- 14% (bradykinin) and 70 +/- 20% (oxytocin) as compared with basal conditions, whereas ASP+ accumulation was slightly reduced in LLC-PK1 cells after stimulation with DOG (1 mumol/l, -20 +/- 7%, n = 10) and angiotensin II (0.1 nmol/l, -20 +/- 5%, n = 6). ASP+ accumulation in IHKE-1 cells also was increased by 0.5 mumol/l (20 +/- 8%, n = 8) and 1 mumol/l forskolin (35 +/- 13%, n = 19), and by 8-bromo-cAMP (1 mumol/l, 125 +/- 25%, n = 9), both activators of the cAMP-dependent protein kinase (PKA). Activation of the cGMP-dependent protein kinase (PKG) by human atrial natriuretic peptide (10 nmol/l, n = 10) or 8-bromo-cGMP (0.1 mmol/l, n = 12) resulted in an increase of 35 +/- 5% and 28 +/- 6%, respectively. Activation of PKA and PKG had no influence on ASP+ transport in LLC-PK1 cells. Regulation of ASP+ uptake by these two cell lines may be caused by direct phosphorylation of the organic cation transporters involved or by regulation of trafficking of the transporters to the membrane. Differences in the organic cation transporter isoforms or alternatively, in the trafficking may contribute to the distinct regulation of ASP+ transport in IHKE-1 and LLC-PK1 cells.

Animals↗
PubMed1997

Moxonidine inhibits Na+/H+ exchange in proximal tubule cells and cortical collecting duct.

The imidazoline receptor agonist moxonidine has been recently introduced as an antihypertensive therapy. Imidazoline specific binding sites have also been found in the kidney. Moxonidine induced natriuresis and diuresis in clearance studies in rats. Related substances such as various guanidinium derivatives have been shown to inhibit Na+/H+ exchange in several preparations. We therefore examined whether the renal effects of moxonidine could be mediated by an inhibition of the Na+/H+ exchanger. Intracellular pH (pHi) was measured microfluorimetrically with BCECF in proximal LLC-PK1 cells and in the principal cells of rat cortical collecting ducts (CCD). In LLC-PK1 cells moxonidine (10 mumol/liter) had no effect on the basal pH1; however, it reduced the Na+/H+ activity reversibly by 43 +/- 4% (N = 26) when the exchanger was activated by cellular acidification. In rat CCD cells moxonidine slightly decreased basal pHi by 0.08 +/- 0.03 pH units (N = 12). After acidification the recovery rate of pHi was reduced with moxonidine by 45 +/- 6% (N = 18). The effects of moxonidine could be mimicked in both cell types by inhibitors of the Na+/H+ exchanger (HOE 694, amiloride). In the presence of the imidazoline receptor antagonist idazoxan (10 mumol/liter) the effects of moxonidine were almost completely inhibited. The alpha 2-antagonist yohimbine (10 mumol/liter) did not significantly alter the effects of moxonidine in both cell types. These data suggest that in LLC-PK1 and in rat CCD cells, Na+/H+ is inhibited by moxonidine via an activation of the imidazoline receptor.

Adrenergic alpha-Antagonists↗
PubMed1997

Elemental mercurial poisoning.

A 39-year-old man injected 40 mL of elemental mercury in an attempted suicide 3 years before coming to our facility. No specific treatment regimen had been done since then. Chest x-ray films showed mercury deposits in the lungs, as well as around the injection site. The mercury concentration in his blood was at 96.3 micrograms (0.480 nmol/L), thus significantly elevated (given a reference range of up to 2 micrograms Hg/L), as was the renal mercury elimination. Despite mercurial deposits within the pulmonary circulation, the pulmonary function showed normal values, with no reduction of the diffusion capacity. There were signs of polyneuropathy. The patient was given sodium dimercaptopropanesulfate (Dimaval) for mercury complexation. This case report outlines the diagnosis and therapy for mercurial poisoning through metallic mercury.

Adult↗
PubMed1997

Influence of proteinuria on long-term transplant survival in kidney transplant recipients.

Long-term prognosis in kidney transplant recipients depends on multiple factors. To investigate whether mild proteinuria within the first 6 months following transplantation is a determinant of the long-term function and survival of kidney transplants, 357 patients transplanted between 1980 and 1990 were retrospectively examined over a period of 5 years. 25.5% of the patients developed an early proteinuria between 0.25 and 1.0 g/day over 6 or more months. This group was well matched concerning gender, age of recipient, underlying disease, time on hemodialysis, donor age, cold ischemia time and HLA mismatches with the group without proteinuria (n = 266). Five-year transplant survival in the group with proteinuria was 58.9% in contrast to 85.6% in recipients without proteinuria. Intermittent proteinuria did not worsen long-term prognosis. Proteinuria of 12 months or longer further reduced 5-year transplant survival to 42.6%. Over the whole observation period, serum creatinine in recipients with proteinuria was about 0.5 mg/dl higher as compared with patients without proteinuria. No correlation between proteinuria and gender, age of recipient, duration of hemodialysis, age of donor, cold ischemia time and mismatches could be detected. In conclusion, early proteinuria apparently is not due to established donor or recipient factors. However, there is a strong correlation of proteinuria with worse transplant function and survival.

Adult↗
PubMed1997

Effects of moxonidine and clonidine on renal function and blood pressure in anesthetized rats.

Using classical clearance techniques, the renal effects of moxonidine and clonidine were studied in the rat. Moxonidine (0.25 and 0.5 mg/kg body weight i.v.) increased transiently fractional fluid and Na+ excretion. Similarly, clonidine in the same i.v. doses caused a sustained increase in fractional fluid excretion, but only a short lasting increase in fractional Na+ excretion that was similar to the effect of moxonidine. Water diuresis experiments showed that the agonists mostly exert their actions within the proximal tubule. Antagonists such as idazoxan and yohimbine did not change fractional fluid excretion and Na+ excretion by their own. Both, the nonselective imidazoline/alpha 2-adrenoceptor antagonist idazoxan and the pure alpha 2-adrenoceptor antagonist yohimbine attenuated the moxonidine induced effects on fractional fluid excretion and Na+ excretion. The clonidine induced increase in fractional fluid and Na(+)-excretion was inhibited by yohimbine and desmopressin only. The effects on systemic blood pressure after moxonidine or clonidine application were similar. The initial blood pressure increases after moxonidine application, however, was less than with clonidine, whereas the hypotensive potency was more pronounced. Similar to the effects on kidney function, idazoxan and yohimbine had no influence on systemic blood pressure by themselves. Immediately after moxonidine application, a short lasting increase in renal plasma flow and glomerular filtration rate could be observed. Our results demonstrate, that moxonidine exerts renal effects, which are different from those of clonidine. At present time, renal effects mediated by imidazoline receptors and alpha 2-adrenoceptors cannot be clearly distinguished.

Adrenergic alpha-2 Receptor Agonists↗