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PubMed1986

[Analgesic nephropathy].

Analgesic nephropathy, its morphology, development and pathogenesis are described. The earliest analgesic-caused lesion is capillary sclerosis of the urinary tract mucosa. Later focal necroses can be found in the papillae surrounding the collecting ducts. Foci of necrosis progress and become confluent, resulting in complete papillary necrosis. Later renal cortical lesions develop due to retained areas of papillary necrosis. The cortical changes include chronic interstitial nephritis with cortical atrophy in the suprapapillary region as well as hypertrophy of the columnae Bertini with segmental, focal glomerulosclerosis. The analgesic-related lesions are the result of toxic damage to endothelial, tubular and interstitial cells. Analgesic-induced kidney and urinary tract changes are quite specific. Frequent complications include hypertension, pyelonephritis, hydro- or pyonephrosis and urinary tract tumors. The clinical picture is characterized by the consequences of distal tubular damage: impairment of urine concentrating capacity, acidosis, electrolyte loss. Analgesic nephropathy is an example of an absolutely preventable drug induced nephropathy. It is the most important single manifestation of the analgesic syndrome. It is recommended that prescriptions for mixed analgesics (multi-component analgesics) should be made obligatory. Monocomponent analgesics could be sold over-the-counter.

Analgesics↗
PubMed1986

[Quantitative pathomorphological findings in chronic glomerulonephritis at autopsy: characterization of the grade of renal insufficiency for correlation studies].

The investigation is based on 49 autopsies at which chronic glomerulonephritis (GN) was found. The glomerular findings were classified by the WHO classification of renal diseases. The ratio of kidney weight (g) to body height (cm) gave a constitutional kidney index which correlated with the degree of global and segmental (more than 50%) sclerosis of glomeruli in chronic GN (diffuse intracapillary type). The negative correlative coefficient from simple linear regression was rho = -0.606. Chronic GN was then further subdivided into four groups which mutually correlate: diffuse sclerosing GN (so-called end-stage kidney). Index: 0.27 g/cm; diffuse sclerosing GN (over 80% glomerular sclerosis). Index: 0.49 g/cm; diffuse proliferative and extensive sclerosing GN (more than 50% and less than 80% sclerosis) Index: 0.59 g/cm; diffuse proliferative and mild to moderate sclerosing GN (less than 50% sclerosing). Index: 0.93 g/cm. The indices of the diffuse extracapillary GN were high in comparison with diffuse intracapillary GN. The kidney index of diffuse extracapillary proliferative and extensive sclerosing GN with over 80% fibrous crescents was 0.78 g/cm. Index of diffuse extracapillary proliferative and mild to moderate sclerosing GN, mostly epithelial and fibro-epithelial, few fibrous crescents was 1.30 g/cm. The mean values of the indices for normal kidneys were (males) 0.78-0.81 g/cm and (females) 0.73-0.75 g/cm (age: 20-60 years). These results may be used for correlative investigations with morphometric parameters of renal osteopathy.

Adolescent↗
PubMed1979

[Report on renal transplant patients. Ocular changes due to renal disease and immunosuppressive therapy (author's transl)].

51 patients with renal transplants were examined ophthalmologically 31,1 (1--77) months after the transplantation. 80,4 p. c. showed ocular complications: cataract formation in 43,1 p. c. of the patients examined and increased intraocular pressure values between 22 and 30 mm Hg in 3 patients are to be attributed to the systemic immunosuppressive therapy. Further ocular changes were recurrent subconjunctival haemorrhages due to increased vascular rigidity, calcium phosphate deposits in the conjunctiva due to persistant secondary hyperparathyroidism and fundus changes (pigmentary irregularities in the foveal regions, narrow arterial vessels). Although marked arterial hypertension was observed in 21 patients after the transplantation, no signs of hypertensive retinopathy could be found. Despite the high incidence of ocular complications after renal transplantation the risks of immunosuppressive therapy must be considered as tolerable: cataract formation and increased intraocular pressure do not impair the positive effect of renal transplantation on ocular functions. Regular ophthalmological control examinations of renal transplant patients are advisable.

Adolescent↗
PubMedDate not supplied

Renovascular hypertension: pathophysiology, diagnosis, and treatment.

Renovascular hypertension can result from renal artery lesions involving the main renal artery, or its branches. It is generally felt that the elevation of blood pressure results from excessive systemic vasoconstriction secondary to enhanced renin secretion by one or part of one kidney. Renin secretion is enhanced because of constriction of the renal artery and resultant intrarenal ischemia. Clinically patients cannot be distinguished from those with essential hypertension and diagnosis must be made with arteriography although urography and isotope renography may suggest the diagnosis. Surgical cure can be predicted if differential renal vein renin ratios lateralize but a non-lateralizing study does not necessarily mean that surgery will fail. In properly selected patients, surgical results are excellent.

Adolescent↗
PubMed1979

[Kidney in chronic arterial hypertension: "resetting" and the role of the renal medulla in its development].

In the system of long-term maintenance of the arterial pressure level by means of the renal excretion mechanism described by Guyton et al., the renal medulla with its counterflow-concentrating multiplier and powerful source of natural natriuretics, the prostaglandins, plays the role of a "control device", a regulator setting the level of arterial pressure required for fulfilling the complete volume of renal excretion of salts and water. Increase in systemic arterial pressure causes the development of a complex of structural-functional changes in the kidney, the common purpose of which consists in preventing the loss of salts and water by the organism by shifting parameters of the excretory renal function in such a manner that the normal (balanced with the supply of salts and water to the organism) volume of excretion may occur with higher values (kidney "resetting"). The central role in accomplishing this "resetting" is played by the medullary excretory mechanism which is closely connected, due to the absence of autoregulated blood flow in the medulla, with systemic arterial pressure. When the kidney reaches the "resetting" this mechanism provides for a sufficiently full volume of excretion only when the arterial pressure increases, maintaining its fixed (higher) level by means of the feedback mechanism. In hypertension caused by overdosage of corticosteroid hormones or excess of salt in the diet the increase of pressure develops as a compensation for the occurring deficiency of the medullary excretory mechanism.

Angiotensin II↗
PubMed1985

Deterioration in renal function in patients with chronic renal failure after treatment with captopril.

Acute reversible renal failure has been reported in patients receiving captopril, especially those with unilateral or bilateral renal artery stenosis. Two patients with advanced renal disease presented with an acute deterioration in renal function after the introduction of captopril treatment. In both instances this deterioration was irreversible. Captopril should be used with caution in patients with advanced renal disease.

Aged↗
PubMed1977

[Morphology of diabetic nephropathy (author's transl)].

Renal complications occur frequently in diabetics. Glomerular lesions exist in basal membrane thickening, diffuse and nodular glomerulosclerosis, exudative lesions and glomerular aneurysms. Tubular and interstitial changes are characterized by Armanni-Ebstein cells, by pyelonephritis and papillary necroses. Vascular changes occur in the form of arteriosclerosis and arteriolosclerosis. Nodular glomerulosclerosis is characteristic of diabetic renal damage, all other changes only occur more frequently in diabetics. Recently, studies deserve attention which suggest a regression of glomerular lesions if the diabetic metabolism is normalized.

Aneurysm↗
PubMed1977

[Clinical aspects of diabetic nephroangiopathy (author's transl)].

Diabetic nephropathy is a dangerous and insidious complication of diabetes mellitus. The course is variable and from the statistical point of view usually unfavorable. The pathogenesis of the complaint is not fully known. Of the numerous hypotheses, the one most favored is a defective glucose metabolism with uncontrolled inundation of the kidney cells with glucose. The predominant symptom is proteinuria. Early recognition and optimal correction of the metabolic disorder may possibly delay the manifestation of diabetic nephropathy for a time. The use of Somatostatin is attracting great attention today. With such a preparation, the stabilization of diabetes could be facilitated.

Adolescent↗