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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 649 records · Page 36Linked to original sources

[New aspects of calcium metabolism in kidney calculus disease].

Recurrent calcium stone disease appears to be related to a high dietary intake of animal protein. The following mechanisms have been discussed to explain the relationship between dietary protein and calciuria: increased glomerular filtration rate (GFR), increased rate of sulphate excretion, acidosis-induced increase in ionised serum calcium ("filtered load") and decrease in tubular reabsorption, and mobilisation of bone mineral. Protein also diminishes urinary citrate. However, it has not been established in controlled trials whether a reduced dietary intake of protein diminishes the recurrence rate of renal stones. Determination of the normal range of urinary calcium is dependent on numerous variables: size; GFR; age; excretion of Na, Mg and Pi; dietary intake of Ca and protein; season. Ideally, all these variables should be evaluated. In many patients with recurrent stone formation hypercalciuria will be found. There is a consensus of opinion that intestinal Ca absorption is increased, but elevated frequency of a renal Ca leak has not been established. For patient management discrimination between absorptive and resorptive hypercalciuria is important; a simple test that can be performed as an outpatient procedure is proposed in order to make this distinction.

Calcium↗

[New aspects of endocrine regulation of calcium metabolism].

The maintenance of circulating calcium levels within the narrow physiological range requires the action of two hormones, the polypeptide hormone parathyroid hormone and the steroid hormone 1-alpha-25-dihydroxyvitamin D3. These two hormones act on bone, kidney and intestine to regulate calcium homeostasis. Disorders of mineral metabolism are frequently associated with abnormal regulation of the metabolism of parathyroid hormone or 1-alpha-25-dihydroxyvitamin.

Calcitriol↗

[Cystic kidney].

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Adult↗

[Diabetic nephropathy in type II diabetes: effect of metabolic control and blood pressure on its development and course].

The influence of metabolic control and blood pressure on the onset and course of clinical nephropathy (persistent proteinuria) was investigated in 63 type II diabetics with persistent proteinuria and a corresponding group without proteinuria. Diabetics with a later onset of persistent proteinuria had, even in the pre-proteinuria stage, higher blood pressures than diabetics without proteinuria. There was an inverse relationship between blood pressure and the interval between the diagnosis of diabetes and the onset of persistent proteinuria. There was no difference in metabolic control between diabetics with and those without later development of persistent proteinuria. However, for patients with clinical nephropathy there was a weak inverse correlation between blood pressure levels during the preproteinuric stage, on one hand, and the interval between diabetes diagnosis and onset of persistent proteinuria, on the other. Poor metabolic control and hypertension during the proteinuric stage were associated with rapid deterioration of renal function.

Blood Pressure↗

[Conversion enzyme inhibitors in the antihypertensive treatment of patients with renal insufficiency].

Changes in serum creatinine concentration and proteinuria over a period of 12 months were analysed retrospectively in hypertensives in renal failure, 39 treated with conversion-enzyme inhibitors and 41 treated with other antihypertensives. The occasionally recorded blood pressures were comparable in the two groups. Median serum creatinine levels in the patients treated with conversion-enzyme inhibitors rose from 2.33 mg/100 ml (range 1.5-5.5) after one month acutely by 0.4 mg/100 ml and then remained essentially constant. In nine patients the level was higher by greater than or equal to 0.5 mg/100 ml after 12 months than at the beginning of treatment. Proteinuria did not show any identifiable changes. On the other hand, in those patients treated with other antihypertensives, median serum creatinine concentration rose gradually over 12 months from 2.4 mg/100 ml (range 1.5-6.0) to 3.45 mg/100 ml (1.5-12.9). In 18 patients the serum creatinine level rose by less than or equal to 0.5 mg/100 ml. Five patients developed side effects to conversion-enzyme inhibitors, but none required discontinuation of treatment. It is concluded that the use of conversion-enzyme inhibitors in patients with renal failure is effective and largely safe. It apparently causes less of a rise in serum creatinine than other antihypertensives.

Adrenergic beta-Antagonists↗

[Acute granulomatous interstitial nephritis with iritis. Possible induction by non-steroidal antiphlogistics].

A 49-year old woman developed non-oliguric acute renal failure accompanied by bilateral acute anterior uveitis, following a three weeks' period of lethargy, anorexia and temporary fever. Kidney biopsy revealed acute interstitial nephritis with interstitial infiltrations of lymphocytes and monocytes, as well as multiple perivascular epithelioid granulomas. A substantial improvement of renal function was achieved under treatment with systemic corticosteroids. The uveitis resolved completely under additional topical treatment. During a follow-up period of 9 months, there has been no relapse of nephritis or uveitis. The disease of this patient resembles the so-called TINU syndrome of unknown aetiology. Remarkable features of the present case are the histological diagnosis of granulomatous acute interstitial nephritis in the absence of systemic granulomatous disease, as well as a possible association with the administration of non-steroidal antiinflammatory drugs.

Acute Disease↗

Familial glomerulonephritis.

Between 1970 and 1984, the diagnosis of glomerulonephritis was made in 860 patients on the basis of a nephritic sediment and/or renal biopsy; of these patients, 86 (10%) had at least one first-degree relative with glomerulonephritis. These patients originated from 45 families and 1674 family members were screened; 172 had glomerulonephritis, of whom 101 could be classified. The diagnostic breakdown of the 101 patients showed that 50.5% had classical Alport's syndrome; 21.8% had atypical forms; 17.8% had familial IgA glomerulonephritis; 1.9% had focal segmental glomerulosclerosis with Wolff-Parkinson-White syndrome; and 7.9% had benign familial haematuria. The proportion of patients with glomerulonephritis who had familial disease was higher than expected. The family history is an important point to consider in the examination of patients with glomerulonephritis.

Adolescent↗