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Biomedical subjects

A Luger

Publications and source records attributed to A Luger.

At least 37 records · Page 2Linked to original sources
PubMed2000

Growth hormone replacement therapy is not associated with retinal changes.

GH and/or growth factors are thought to play a role in the pathogenesis of diabetic retinopathy. In addition, the occurence of retinal changes mimicking diabetic retinopathy in two GH-deficient (GHD) patients receiving GH replacement therapy (GHRT) has recently been reported. The present study was performed to evaluate whether this was a coincidence or whether GHRT might regularly induce retinal changes. Sixty-one GHD patients on GHRT with a mean age of 42.5 +/-17.3 yr were examined by one ophthalmologist (AR). The mean duration of GHRT was 8.4 +/- 3.7 yr in childhood onset and 3.5 +/- 2.1yr in adult onset patients. Plasma insulin-like growth factor I concentrations were 76.4 +/- 49.6 ng/mL before GHRT and 244.3 +/- 119.2 ng/mL while receiving GHRT with a dose of 1.7 +/- 0.7 IU/day. After pupil dilatation with tropicamide, fundus examinations of both eyes were performed using a Volk 90 diopter fundus lens with a slit lamp (Haag Streit, Bern, Switzerland). In none of the patients were vascular or retinal changes like macular edema, microaneurysms, hemorrhages, hard exsudates, cotton wool spots, preproliferative signs, or proliferations found. The optic discs were also normal in all patients. We conclude, therefore, that long-term GHRT can be administered safely in GHD patients without an increased risk of retinal changes.

Adolescent↗
PubMed1998

Effect of long-term growth-hormone substitution therapy on bone mineral density and parameters of bone metabolism in adult patients with growth hormone deficiency.

Reduced bone mineral density (BMD) and the prevalence for osteoporotic vertebral fractures are symptoms of growth hormone deficiency (GHD) syndrome, and GH replacement therapy is now available for GH-deficient adults. We investigated the long-term effects of GH replacement therapy on bone mineral density (BMD) and bone metabolism in 19 adult patients with GHD over a period of 18 months. In response to GH treatment, the initially decreased IGF-I concentrations rose significantly during 18 months of therapy to levels within the normal range (matched for sex and age) (mean change 158.1 +/- 50.8 ng/ml, P < 0.001). Parameters of bone formation such as osteocalcin (OC) and procollagen I-C-Peptide (PICP) showed a significant increase in the first 6 months of therapy, followed by a slight decrease in the next months. Markers of bone resorption (CrosslapsR and deoxypyridinoline (D-Pyr) also increased significantly with a peak value after 6 months and all parameters except PICP remained above baseline values after 18 months. BMD of the femoral neck (FN) showed an increase after 18 months of therapy (mean change 0.01 +/- 0.03 g/cm2 after 18 months, n.s.). However, the increase in BMD was significant only in the lumbar spine (LS) (mean change 0.03 +/- 0.04 g/cm2, P < 0.05 after 18 months). We conclude that GH replacement therapy in adult patients with GHD over a period of 18 months causes a pronounced increase in bone turnover mainly during the first 12 months of therapy and increases BMD of the lumbar spine and the femoral neck after 18 months.

Adult↗
PubMed1998

Effects of parathyroid hormone and serum calcium on the phenotype and function of mononuclear cells in patients with primary hyperparathyroidism.

BACKGROUND: Several studies have demonstrated specific influence of parathyroid hormone (PTH) on immune parameters, especially on T- and B-cell function, migration of polymorphonuclear leucocytes (PMNLs) and antibody synthesis, in patients with secondary hyperparathyroidism and chronic renal failure and recently also in patients with primary hyperparathyroidism (pHPT). METHODS: We therefore examined 12 patients with pHPT before and 6 months after parathyroidectomy (PTX) and nine sex- and age-matched control subjects to determine the impact of PTH and serum calcium concentrations on several immune parameters, including (a) serum concentrations of immunoglobulins, (b) immunophenotype of peripheral blood lymphocytes, (c) phytohaemagglutinin (PHA)-induced lymphocyte proliferation and (d) monocytic surface marker expression. RESULTS: Serum concentrations of immunoglobulins (IgG, IgA, IgM) were unaffected by elevated serum PTH and calcium levels. T lymphocytes (CD3), B lymphocytes (CD19), NK cells (CD16/56) and monocytes (CD16) revealed a normal distribution and were not different before and after PTX in patients with pHPT when compared with the control group. CD4+ T-helper lymphocytes were significantly elevated pre- and post-operatively in patients with pHPT. The lymphocyte proliferation response to PHA in the highest concentration (12.5 micrograms L-1) tested was significantly suppressed in patients with pHPT preoperatively when compared with the patients post-operatively and the control group. In addition, both CD4+ and CD8+ lymphocytes showed a lower expression of activation markers, interleukin 2 (IL-2) receptor (CD25) and transferrin receptor (CD71), which could be partially restored 6 months after PTX, but did not reach normal values. CONCLUSION: In summary, in contrast to the findings in patients with secondary HPT, pHPT appears to be associated with less alterations of immune functions. Chronically elevated serum PTH and calcium concentrations in patients with pHPT induce a higher percentage of CD4+ helper T lymphocytes and a suppressed lymphocyte response to PHA as well as a reduced expression of activation markers on peripheral blood lymphocytes.

Adult↗
PubMed1998

Adrenal function in patients with chronic renal failure.

Previous studies have reported divergent findings on the function of the hypothalamic-pituitary-adrenal axis in patients with chronic renal failure (CRF). The low-dose adrenocorticotropin (ACTH) test offers the possibility of unmasking adrenal dysfunction, which might remain undiscovered using the ACTH test with the standard 250-microg dose. Furthermore, the choice of renal replacement therapy (either hemodialysis or continuous ambulatory peritoneal dialysis [CAPD]) might have an impact on adrenal function. To investigate these possibilities, ACTH tests were performed with three different doses (ie, 1, 5, and 250 microg) in 14 CRF patients and in seven healthy controls. Seven of the CRF patients were receiving chronic hemodialysis and seven were receiving CAPD. Basal plasma concentrations of cortisol were comparable in the three groups tested (5.3+/-0.4 microg/dL in the controls, 6.6+/-0.7 microg/dL in the hemodialysis patients, and 7.9+/-1.0 microg/dL in the CAPD patients), whereas basal ACTH concentrations were significantly elevated in the CRF patients (28.5+/-3.8 pg/mL in the hemodialysis patients and 33.0+/-6.0 pg/mL in the CAPD patients) when compared with normal controls (17.0+/-1.4 pg/mL; P < 0.05). All three doses of ACTH resulted in a rapid increase of plasma cortisol concentrations that was comparable in all three groups. In the hemodialysis patients, a trend toward a diminished response to the lowest dose of 1 microg was noticed. We conclude, therefore, that adrenal response to ACTH in various doses is unaffected in CRF independent of whether hemodialysis or CAPD is chosen for renal replacement therapy.

Adrenal Glands↗
PubMed1997

Effect of elevated serum prolactin concentrations on the immunophenotype of human lymphocytes, mitogen-induced proliferation and phagocytic activity of polymorphonuclear cells.

It has been suggested that the immune system is an important target tissue of prolactin (PRL). We therefore investigated several immune parameters in nine patients with chronically elevated serum prolactin concentrations. The immunophenotype of lymphocytes, mitogen-induced lymphocyte proliferation and phagocytic activity of polymorphonuclear cells were determined under high serum prolactin levels and 2 weeks after treatment with dopamine agonists. An increased CD4/CD8 ratio in the hyperprolactinaemic patients could be detected compared with healthy control subjects, which remained high after treatment and did not seem to correlate with serum prolactin concentrations. Peripheral blood B lymphocytes showed an increased expression of CD69 in the treated group but not in untreated patients compared with healthy control subjects. Interleukin 2 receptor, CD45RO, transferrin receptor or HLA-DR expression of CD4 or CD8 cells, as well as oxidative burst and phagocytic activity of granulocytes, were not affected in the patients with prolactinomas. Lymphocyte transformation response to phytohaemagglutinin in vitro was found not to be influenced by elevated prolactin levels except at the highest mitogen concentration tested. These data together with previous reports suggest that, although PRL is required for lymphocyte maturation to achieve normal immune function, elevated PRL levels do not lead to an 'overstimulation' of the immune system in men.

Adult↗
PubMed1997

Effect of successful parathyroidectomy on hematopoietic progenitor cells and parameters of red blood cells in patients with primary hyperparathyroidism.

Elevated levels of parathyroid hormone (PTH) in primary and secondary hyperparathyroidism inhibit hematopoiesis at the level of hematopoietic progenitor cells, mainly the burst forming units-erythroid (BFUe). Removal of parathyroid adenomas is associated with an increase in hematopoietic progenitor cells. In contrast, a certain amount of PTH and calcium is needed to correct anemia after bleeding demonstrating that PTH has also a stimulatory effect on the bone marrow. We examined the effect of parathyroidectomy (PTX) in 10 patients with histologically proven primary hyperparathyroidism on hematopoietic progenitor cells and several parameters of red blood cells before and at 5, 30 and 90 days after PTX. After successful surgery serum levels of iPTH (p < 0.01) and calcium (p < 0.001) decreased significantly. Subsequently a steady increase in all hematopoietic progenitor cell classes was observed reaching significance for BFUe only (p < 0.05). Red blood cells and hemoglobin reached nearly pretreatment values within 90 days after PTX after they had decreased due to surgery associated blood loss. 8 patients undergoing hemithyroidectomy without PTX showed a similar decrease in red blood cells and hemoglobin followed by a rise after the operation. The changes of these parameters did not differ significantly from the patients with pHPT. In contrast to the patients with pHPT, no changes in hematopoietic progenitor cells during the 90 days were observed. The presented data provide further evidence that increased PTH concentrations might inhibit hematopoiesis in humans in vivo. The inhibition can be reversed following PTX by normalisation of PTH concentrations.

Aged↗
PubMed1997

The long-acting dopamine agonist bromocriptine mesylate as additive immunosuppressive drug after kidney transplantation.

BACKGROUND: Acute rejection is an important risk factor for kidney graft loss. As evidence suggests that prolactin has important immunostimulatory properties, we conducted a randomized, prospective open trial in which bromocriptine, a drug suppressing prolactin secretion, was administered as an additive immunosuppressive drug after first cadaver kidney transplantation. METHODS: In the treatment group bromocriptine was given intramuscularly to 22 patients after their first kidney transplantation along with conventional immunosuppression (cyclosporin A, glucocorticoids). Twenty-three patients receiving only conventional immunosuppression served as control subjects. The incidence of acute graft rejections, graft losses, and infections was evaluated. RESULTS: Serum prolactin concentrations were slightly elevated above normal values before transplantation (32 +/- 5.3 ng/ml) and decreased to values between 13 and 16 ng/ml in the control group and were totally suppressed in the bromocriptine group. After 6 months of follow-up overall patient and allograft survival was 97.7% and 91% respectively. Acute rejection episodes occurred in 31 patients (77.5%): 15 in the bromocriptine group vs 20 in the control group (n.s.). In each group eight patients experienced a cytomegalovirus infection. The incidence of severe bacterial infections (i.e. pneumonia and sepsis) was five and six respectively. The necessity of haemodialysis after transplantation was 3.1% in the patients on bromocriptine and 23% in those without. CONCLUSIONS: Suppression of circulating prolactin concentration by bromocriptine did not improve the clinical outcome of patients after kidney transplantation receiving cyclosporin and prednisolone.

Acute Disease↗
PubMed1996

The influence of growth hormone substitution therapy on erythroid and myeloid progenitor cells and on peripheral blood cells in adult patients with growth hormone deficiency.

It has been reported that hypophysectomized rats exhibit normochromic, normocytic anaemia. Pancytopenia with impaired DNA synthesis in the bone marrow can be restored in these hypophysectomized rats by syngeneic pituitary grafts placed under the kidney capsule or treatment with growth hormone (GH). Until now, adults with hypopituitarism have received adequate replacement therapy with thyroxine, cortisol and sex steroids, but not with GH. We therefore investigated the effects of GH replacement therapy on the proliferation and differentiation of erythroid and myeloid progenitor and peripheral blood cells in 11 adult patients with growth hormone deficiency in a double-blind, placebo-controlled study for the first 6 months of therapy. The placebo group showed no changes during the first 6 months without therapy in either insulin-like growth factor I (IGF-I) levels, erythroid and myeloid progenitor precursor cells or peripheral blood cells. After commencement of GH therapy, IGF-I levels rose significantly during 24 months of therapy from 75.3 +/- 13.5 to 225 +/- 34.7 ng mL-1 (P < 0.001). Erythroid and myeloid progenitor precursor cells showed a steep and significant increase after 18 and 24 months of therapy (erythroid: from 10.7 +/- 3.5 to 261.4 +/- 79.8, P < 0.02, after 18 months and to 276.8 +/- 149.8 x 10(5) mononuclear cell colonies, P < 0.03, after 24 months; granulocyte-macrophage colony-forming units: from 39.7 +/- 9.8 to 316.9 +/- 124.6, P < 0.002, after 18 months and to 366 +/- 188.7 x 10(5) mononuclear cell colonies, P < 0.03, after 24 months), whereas the peripheral red and white blood cells exhibited only minimal non-significant changes. The principal regulators of erythropoiesis, such as erythropoietin, and parameters reflecting erythropoiesis in the peripheral blood, such as reticulocytes, remained almost unchanged throughout the whole study period. We therefore conclude that patients with GH deficiency do not have anaemia, but have haematopoietic precursor cells in the lower normal range, and that GH substitution therapy over a period of 24 months has a marked effect on erythroid and myeloid progenitor precursor cells but only negligible effects on peripheral blood cells in GH-deficient adults.

Adult↗
PubMed1996

Anterior pituitary function in patients with newly diagnosed rheumatoid arthritis.

Hormonal dysfunction involving the hypothalamic-pituitary-adrenal (HPA) axis, prolactin (PRL) secretion and sex hormone status has been supposed to contribute to the development or persistence of rheumatoid arthritis (RA). In addition, a reduced number of glucocorticoid receptors on circulating lymphocytes has been found in patients with RA. However, so far most studies have been performed in pre-treated patients. A combined test for total anterior pituitary reserve was performed in 10 patients with newly diagnosed untreated RA. Before and after stimulation with the respective hypothalamic releasing hormones, RA patients showed no difference in plasma concentrations of adrenocorticotrophic hormone (ACTH), cortisol, prolactin (PRL) and thyroid-stimulating hormone (TSH) when compared to healthy controls. In contrast, the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) was blunted in RA patients. The hypothalamic-pituitary-thyroid/gonadal and adrenal axes seem to be unaltered in RA. However, if one considers the presence of chronic inflammation, normal plasma ACTH and cortisol concentrations must be considered as inappropriately low. The observed blunted GH release could be mediated by cytokines (e.g. IL-1), which are known to be elevated in RA.

Adrenocorticotropic Hormone↗
PubMed1996

Detection of Borrelia burgdorferi-specific DNA in urine specimens from patients with erythema migrans before and after antibiotic therapy.

A nested PCR was developed for the detection of Borrelia burgdorferi-specific DNA in the urine of patients with erythema migrans. The target for the nested PCR was a specific region of the flagellin gene; the detection limit was less than five organisms of B. burgdorferi including all three species B. burgdorferi sensu stricto, B. afzelii, and B. garinii. A prospective, controlled, blinded study was performed with 26 patients with erythema migrans to evaluate the nested PCR method with clinical samples. B. burgdorferi-specific DNA could be detected in urine specimens from 22 of 24 patients with erythema migrans (sensitivity, 91.61%). Immediately after therapy, 11 of 19 patients still yielded positive results (58%). Eight weeks after therapy, 2 of 16 patients (13%) were positive by PCR of urine, and 20 weeks after treatment none of seven investigated urine samples was reactive. Essential for the sensitivity that was obtained was the development of a simple DNA extraction procedure. The results of the study indicate that the described method is highly sensitive and allows for the effective control of the efficacy of antibiotic therapy in patients with early Lyme borreliosis.

Adult↗
PubMed1996

Dopamine D2 receptor imaging in pituitary adenomas using iodine-123-epidepride and SPECT.

UNLABELLED: Epidepride is a novel benzamide derivative with high affinity for D2 receptors. Epidepride, in its 123I-labeled form, can be used for SPECT imaging of striatal and extrastriatal dopamine D2 receptors. The present study evaluated the usefulness of epidepride and SPECT for in vivo imaging of dopamine receptors in pituitary adenomas. METHODS: SPECT imaging was performed in 19 patients with pituitary adenomas (among them 9 patients had prolactinoma, 4 acromegaly, 4 clinically nonfunctioning pituitary adenoma, 1 Cushing's disease and 1 Nelson's syndrome) and 7 control subjects 180 min after intravenous bolus injection of 3.9 +/- 1.1 mCi [123I]epidepride. The ratio target/cerebellum minus 1, reflecting specific/ nonspecific binding was used as semiquantitative measure of D2 receptor binding. RESULTS: Eight of nine prolactinoma patients demonstrated specific binding within the adenoma. The adenoma/ cerebellum ratio 3 hr p.i. showed a wide variation with values from 2.5-33. In three prolactinomas, binding was higher than in the striatum. Specific binding within the lower range of prolactinomas (adenoma/cerebellum ratios 2 and 4.8) could be demonstrated in two of four GH-secreting adenomas. All four nonfunctioning tumors showed specific binding. The adenoma/cerebellum ratio was within the lower range of prolactinomas (5.2-7.5) in three of these patients but extremely high in one (52.3). No specific tracer uptake could be demonstrated in patients with Cushing's disease or Nelson's syndrome. The striatum/cerebellum ratio 3 hr p.i. in pituitary adenoma patients was not significantly different from control subjects (17.3 +/- 5.5 versus 17.8 +/- 6.6; patients versus control subjects). CONCLUSION: Epidepride appears to be an excellent ligand for in vivo imaging of dopamine D2 receptors in pituitary adenomas. Epidepride SPECT could serve as a predictor for response to dopamine agonist treatment.

Acromegaly↗
PubMed1995

Detection of Borrelia burgdorferi DNA by polymerase chain reaction in the urine and breast milk of patients with Lyme borreliosis.

Current laboratory diagnosis of Lyme borreliosis relies on tests for the detection of antibodies to Borrelia burgdorferi with known limitations. By using a simple extraction procedure for urine samples, B. burgdorferi DNA was amplified by a nested PCR with primers that target the specific part of the flagellin gene. To control possible inhibition of the enzyme (polymerase), a special assay using the same primers was developed. We examined 403 urine samples from 185 patients with skin manifestations of Lyme borreliosis. Before treatment, B. burgdorferi DNA was detected in 88 of 97 patients with Lyme borreliosis. After treatment, all but seven patients became nonreactive. Six of these seven persons suffered from intermittent migratory arthralgias or myalgias, and one from acrodermatitis chronica atrophicans. Two of 49 control patients with various dermatologic disorders and none out of 22 presumably healthy persons were reactive in the PCR. In addition to urine, breast milk from two lactating women with erythema migrans was tested and also found reactive. Borrelia burgdorferi DNA can be detected with high sensitivity (91%) by a nested PCR in urine of patients with Lyme borreliosis. In addition, this test can be a reliable marker for the efficacy of treatment.

Animals↗
PubMed1995

Glomerular function and structure in the sodium-replete and sodium-deplete uninephrectomized spontaneously hypertensive rat: effect of blood pressure reduction, glomerular structure, and blood pressure reduction.

To assess the effects of chronic dietary sodium restriction and blood pressure reduction on glomerular function and structure during the pathogenesis of hypertensive renal disease, experiments were conducted in uninephrectomized (UNX) spontaneously hypertensive rats (SHR) using the dihydropyridine calcium antagonist manidipine. Male SHRs underwent UNX at age 10-11 weeks and subsequently were assigned to one of four groups: sodium-replete (0.4%); sodium-replete and a predetermined antihypertensive dose of manidipine (20 mg/kg body weight); sodium-deplete (0.09%); and sodium-deplete and manidipine (20 mg/kg body weight). Twelve weeks later, renal morphologic and functional studies were performed. Sodium restriction had no significant effect on systolic blood pressure, but creatinine clearance and urinary protein excretion were decreased. Importantly, mean glomerular volume and the prevalence of mesangial expansion were lower with sodium restriction. This occurred in the presence of high concentrations of plasma and renal tissue angiotensin II. Manidipine significantly reduced systolic blood pressure in the sodium-replete and sodium-deplete UNX-SHRs. This therapy was not associated with significant changes in creatinine clearance and urinary protein excretion in the sodium-deplete or sodium-replete UNX-SHRs. The prevalence of mesangial expansion in the sodium-replete UNX-SHR was approximately 50% lower with manidipine. Plasma and renal tissue angiotensin II concentrations were not affected by the drug. In the sodium-deplete UNX-SHR, the prevalence of mesangial expansion was not reduced further by manidipine. However, plasma and renal tissue angiotensin II concentrations were increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Effect of danazol-induced chronic hyperglucagonaemia on glucose tolerance and turnover.

It has been shown that danazol (14-ethinyltestosterone) induces hyperglucagonaemia. To investigate the effect of chronic glucagon excess on carbohydrate metabolism, we studied six patients before and after treatment with danazol for immunothrombopenia. Glucose tolerance and insulin, C-peptide and glucagon secretion during an oral glucose tolerance test (oGTT) as well as peripheral and hepatic insulin sensitivity were determined by means of euglycaemic clamp technique (40 mU m-2 min-1) before and after 3 months of danazol therapy. Overall glucose turnover (Rd) was assessed radioisotopically. (1) Plasma glucagon levels rose significantly from 88 +/- 16 pg mL-1 before to 683 +/- 148 pg mL-1 after therapy (P < 0.01). (2) Glucose levels during an oGTT were not significantly different before and after therapy. Glucose-stimulated insulin secretion at 60 and 120 min and the area under the curve (AUC) for insulin during the oGTT, were significantly increased after danazol treatment compared with pre-treatment values (P < 0.05), whereas glucagon secretion showed a similar decrease at both time points of investigation (NS). (3) Rd during steady state showed a significant decrease during the entire period of euglycaemic clamp following therapy (after 240 min, 3.8 +/- 0.6 vs. 5.3 +/- 0.7 mg kg-1 min-1, P < 0.05). The decline in glucagon during the clamp was similar during steady state before and after therapy. (4) Basal hepatic glucose output did not differ significantly before and after therapy (1.74 +/- 0.41 vs. 1.45 +/- 0.22 mg kg-1, NS), whereas hepatic glucose output during the clamp was significantly less suppressed after danazol therapy. The authors conclude that chronic glucagon excess leads to a decrease in peripheral and hepatic insulin action which is accompanied by an increase in insulin secretion.

Adult↗
PubMed1995

The effects of prolonged substitution of recombinant human growth hormone on renal functional reserve in growth hormone-deficient adults.

Twelve growth hormone (GH)-deficient adults with normal renal function were recruited for a 6-month, double-blind, placebo-controlled study on the effects of prolonged recombinant human growth hormone (rhGH) substitution therapy on renal functional parameters. RhGH was administered at a dose 0.125 IU/kg per week sc the first 4 wk and 0.25 IU/kg per week thereafter. At baseline and after 6 months of therapy, GFR and RPF were measured by the use of iothalamate and para- aminohippurate clearance techniques before and after an intravenous infusion of amino acids (AA) to determine the renal functional reserve capacity (RFRC). At baseline, GFR and RPF were similar in the GH-deficient patients and a group of normal, healthy controls (GFR, 117 +/- 10 mL/min; RPF, 567 +/- 57 mL/min, and filtration fraction, 22 +/- 1.6% in the patient group and GFR, 117 +/- 10 mL/min; RPF, 509 +/- 54 mL/min; and filtration fraction, 24 +/- 1.3% in the control group). GFR increased significantly in the control and patient group after AA infusion; the RFRC, however, was significantly larger in healthy individuals (GFR post-AA infusion, 141 +/- 10 mL in GH-deficient patients and 182 +/- 20 mL/min in controls). Thereafter, six patients received placebo therapy for 6 months and GFR as well as RFRC remained constant (GFR, 107 +/- 9 and 106 +/- 12 mL/min before AA infusion and 132 +/- 14 and 134 +/- 5 mL/min after AA infusion at baseline and after 6 months, respectively). Four patients of the placebo group then continued with rhGH therapy for another 6 months. They and six patients who had rhGH therapy from the beginning form the rhGH treatment study group. During rhGH treatment, plasma insulin-like growth factor activity increased significantly from 93 +/- 17 to 229 +/- 23 ng/mL. Baseline GFR and RPF as well as RFRC were unaltered by the 6 months of rhGH replacement therapy (basal GFR, 124 +/- 7 mL/min before and 123 +/- 9 mL/min after 6 months of rhGH therapy; GFR after AA infusion, 145 +/- 9 mL/min at baseline and 144 +/- 8 mL/min after 6 months of therapy). Kidney size as evaluated by ultrasonography was normal at baseline when compared with that in age- and sex-matched controls (10.3 +/- 0.2 versus 9.9 +/- 0.1 cm) and was unchanged after 6 months of therapy (10.3 +/- 0.3 cm). It was concluded from this study that rhGH substitution for 6 months at a dose of 0.25 IU/kg per week in GH-deficient patients with normal renal function has no adverse functional effects on the kidney.

Adult↗
PubMed1995

Goodpasture's syndrome superimposed on membranous nephropathy. A case report.

We describe a patient with idiopathic membranous glomerulopathy who developed acute deterioration in renal function; this was associated with hemoptysis, severe hypertension, and anti-glomerular basement membrane (anti-GBM) antibody in the serum. Despite aggressive therapy with plasmapheresis, cyclophosphamide and prednisone, the patient progressed to end-stage renal failure and is on maintenance hemodialysis.

Anti-Glomerular Basement Membrane Disease↗