Biomedical subjects
E Ritz
Publications and source records attributed to E Ritz.
Erectile dysfunction in nephrotic syndrome.
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Severe hemorrhagic complications from infection with nephropathia epidemica strain of Hantavirus.
In the following we describe a case of severe hemorrhagic fever with renal syndrome (HFRS) caused by Puumala infection. The diagnosis was made by immunofluorescence technique and by solid phase enzyme immunoassay using recombinant nucleocapsid antigen of a Puumala serotype strain. Such a clinical course with severe bleeding complications is considered untypical for Puumala induced HFRS.
Wegener's granulomatosis, microscopic polyarteritis and pauciimmune crescentic necrotizing glomerulonephritis, an overview.
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Disturbed calcium metabolism in renal failure--pathogenesis and therapeutic strategies.
Absolute or relative deficiency of 1,25(OH)2 vitamin D3 is thought to play a key role in the genesis of secondary (renal) hyperparathyroidism. Elevated concentrations of PTH and--less consistently--diminished concentrations of 1,25(OH)2 vitamin D3 are demonstrable in a considerable proportion of patients with incipient renal failure. Increased PTH concentrations counteract to some extent the trend of 1,25(OH)2 vitamin D3 production to decrease. When iPTH is elevated, prophylactic administration of 1,25(OH)2 vitamin D3 is a logical procedure, even when patients have not yet reached end-stage renal failure. With the use of low doses, the incidence of side effects is low, and excessive lowering of PTH and bone turnover presumably can be avoided. Acute administration of 1,25(OH)2 vitamin D3 to achieve brief episodes of peak plasma levels causes prolonged suppression of pre-pro-PTH mRNA in the parathyroid cell. This provides a rationale to treat symptomatic hyperparathyroidism with intermittent high dose 1,25(OH)2 vitamin D3, either per os or i.v.
Vitamin D metabolism in renal disease. Sir Michael Perrin Lecture 1991.
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New insights into endocrine disturbances of chronic renal failure.
Secondary hyperparathyroidism occurs in the very early stages of renal failure. In the past, there has been considerable controversy concerning the signal triggering secondary hyperparathyroidism. Recently, it has become clear that secondary hyperparathyroidism is, at least to a major extent, the consequence of the deranged endocrine feedback between calcitriol, the secretory product of renal 1-alpha-hydroxylase, and parathyroid hormone. Another recent insight concerns disturbances of the secretion of hypophyseal hormones. These hormones, e.g. GH, gonadotropins and TSH, are secreted in a pulsatile fashion. For all three hormones, reversible abnormalities of secretory rhythmicity have been demonstrated in renal failure. Disturbed oscillatory patterns of hormone secretion provide a new dimension to our understanding of the genesis of endocrine disturbances.
De novo glomerulonephritis in patients during remission from Wegener's granulomatosis.
In a cohort of 20 consecutive patients with Wegener's granulomatosis and biopsy-proven pauci-immune crescentic glomerulonephritis three patients were in remission, but developed again a nephritic sediment without signs of systemic disease or positive ANCA titers. The second renal biopsy showed de novo mesangial IgA deposits 6, 17 and 28 months following admission for systemic disease and institution of immunosuppressive treatment. All patients were male, HLA-DR-2 positive and exhibited repeated upper respiratory tract infections. A fourth patient was admitted in end-stage renal failure with high titers of C-ANCA of the IgG isotype and proteinase 3 ab without clinical evidence of systemic manifestations of WG. Renal biopsy showed chronic sclerosing GN with marked IgA deposits. De novo development of IgA-GN is observed in a remarkable proportion of patients with WG and must be distinguished from exacerbation of the systemic disease.
[Ambulatory 24-hour blood pressure monitoring of children and young adults with autosome dominant polycystic kidney degeneration].
Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent inherited kidney disorder leading to terminal renal failure. About 8% of the dialysis patients suffer from ADPKD, the gene frequency in the general population being about 1:1000. Many facts contribute to the hypothesis that arterial hypertension plays a major role in the pathophysiology of ADPKD. We observed a prevalence of 30% of hypertension in patients with ADPKD and normal serum-creatinine, and of 80% in patients with terminal renal failure. The time of onset of abnormalities of blood pressure regulation is of great interest, since an increase of blood pressure, even in the normotensive range, accelerates the rate of progression. To answer this question, we examined the time of onset of abnormalities in blood-pressure regulation in 23 probands and 23 control patients in a cross-sectional study. The results document abnormal circadian blood-pressure changes and higher blood pressures, although still within the normotensive range, in asymptomatic carriers of the ADPKD-trait, even before and more definitely after onset of puberty. Even at an age when circadian blood pressure is not significantly different, there is an increased LVM as evidence of target organ damage. The findings suggest that (intermittent) increases in blood pressure and blood-pressure-dependent target organ damage precede overt hypertension and renal failure by years or decades.
Non-occlusive mesenteric infarction (NOMI) in dialysis patients--risk factors, diagnosis, intervention and outcome.
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Clinical relevance of albuminuria in hypertensive patients.
Albuminuria (including the form not detectable by conventional tests, i.e., microalbuminuria) as well as renal dysfunction have recently been recognized as important complications in the patient with essential hypertension. The presence of albuminuria predicts cardiovascular events. Albuminuria is associated with more severe hypertension, with evidence of more advanced target organ damage (e.g., left ventricular hypertrophy), and is more prevalent in high-risk groups (e.g., the elderly). On the other hand, albuminuria may also be associated with generalized endothelial barrier dysfunction and thus predispose to accelerated atherogenesis. Ischemic nephropathy from nonmalignant nephrosclerosis has emerged as an important cause of terminal renal failure in the elderly patient with essential hypertension.
Influence of dietary factors on the renal renin-angiotensin system.
Protein meals and infusion of amino acids cause an increase of glomerular filtration rate in humans and animals with normal renal function despite the circulating renin concentration remaining unchanged. The renal hemodynamic response is not altered by angiotensin converting enzyme inhibitors, but it is obliterated by cyclooxygenase inhibitors. By contrast, chronic exposure to high protein diets raises circulating renin and increases messenger RNA of renin (but not of angiotensinogen) in kidney tissue. Chronically high protein intake raises the glomerular filtration rate and reduces glomerular permselectivity; the reverse is seen with low protein intake. In patients with renal failure, acute amino acid infusion or protein meals cause a paradoxical drop in glomerular filtration rate which is not influenced by converting enzyme inhibitors.
How frequent is glomerulonephritis in diabetes mellitus type II?
A high frequency of glomerulonephritis (GN) in diabetics, or coexistence of GN with diabetic glomerulosclerosis, has been reported by previous authors, but the true prevalence of GN in diabetics remains to be established. In the Department of Pathology, Heidelberg, from 1.1.1987 to 31.12.1989 we examined all consecutive patients (89 male, 121 female, median age 74 years; 47-98) who came to autopsy with the diagnosis of "diabetes mellitus" to assess this issue in an unbiased sample. Five patients had known type I diabetes, the others type II diabetes or diabetes of unknown classification. In 61/159 patients, proteinuria had been present (no information in 51 patients) and in 99/169 patients renal failure, i.e. serum creatinine above 1.4 mg/dl (no information in 41 patients). Paraffin-embedded kidney specimens from the upper pole of the left kidney were examined by immunohistochemistry (PAP technique; rabbit antihuman IgG; IgM; IgAab). 166/210 of the patients had glomerulosclerosis by light microscopy (129 diffuse, 37 nodular GS). Concomitant glomerulonephritis, i.e. typical mesangial IgA (and IgG) deposits, with mesangial enlargement by light microscopy were detected in only one case. Membranous GN was not found. These findings must be interpreted against the observation of mesangial immune deposits in 6 of 250 consecutive non-diabetic patients who had come to autopsy [Waldherr et al. 1989]. The findings show that an excessive prevalence of undiagnosed glomerulonephritis in our cohort of elderly type II diabetics was not to be found.
[Insulin--a side issue or indeed the cause of hypertension?].
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Single cell analysis of changes in cytosolic calcium induced by vitamin D3 metabolites in cultured rat mesangial cells.
The acute effects of 1,25-Dihydroxy-vitamin D3 [1,25(OH)2D3] on the concentration of cytoplasmic ionized calcium [Ca2+] of cultured rat mesangial cells were studied at the single cell level by microspectrofluorometry of fura-2-loaded cells. Addition of 1,25(OH)2D3 produced an immediate increase of [Ca2]+. This rise in [Ca2+] was sustained and similar to that caused by the Ca2+ channel agonist BAY K 8644. Comparable changes were also observed in cultured human mesangial cells. The effects of the hormone (10 (-10)-10(-7) M) were dose-dependent (62% and 285%). Only 30-40% of the cells responded to stimulation with 1,25(OH)2D3. 25OHD3 also increased Ca2+ whereas 24,25(OH)2D3 and 1aOHD3 were inactive. Addition of 1 mM CoCl2 or 2-5 microM nifedipine largely blocked the effects of 1,25(OH)2D3 suggesting the involvement of Ca2+ channel activation in the rapid 1,25(OH)2D3-induced increase in mesangial cell [Ca2+]. 45Ca uptake studies are consistent with This interpretation.
[Does the care of diabetic patients with renal failure in the predialysis phase need improvement?].
The cardiovascular risk profile was assessed in all 208 diabetics accepted for dialysis in 28 German dialysis centres from 1985-1987 (104 men, 104 women, mean age 60 [22-82] years). 71 patients had type 1 and 128 type 2 diabetes, and 9 maturity onset diabetes of the young. Of 169 patients, 164 (97%) had hypertension (median systolic blood pressure at start of dialysis 200 [120-280] mm Hg). Only 74 patients (44%) were on continuing anti-hypertensive medication. Median serum cholesterol was 225 (66-424) mg/dl, LDL-cholesterol 158 (43-335) mg/dl and HDL-cholesterol 32 (10-67) mg/dl. In patients with a history of myocardial infarction (n = 26) the median cholesterol concentration was 269 (126-424) mg/dl, while in those with no history of myocardial infarction (n = 132) it was 221 (66-280) mg/dl (P less than 0.05). Only 5% of the patients had received lipid lowering therapy. Out of 175 patients, 65 (37%) had a history of smoking, and 25 (14%) were still smokers at the start of dialysis. There was a strong association between smoking history and amputations. Only 98 of 208 patients (47%) had had a specialist ophthalmological examination in the 12 months preceding the start of dialysis. Proliferative retinopathy was present in 33 out of 53 (62%) type 1 and 15 out of 98 (15%) type 2 diabetics. Out of 22 patients with unilateral or bilateral blindness, 2 (10%) had received no photocoagulation. - This investigation reveals a need for better medical care of diabetics with pre-end-stage renal failure.
Is vasculitis in subacute bacterial endocarditis associated with ANCA?
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Is intermittent oral calcitriol safe and effective in renal secondary hyperparathyroidism?
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