PubMed Health⌕ Search

PubMed · 1134426

[Analgesic nephropathy].

Abstract

Analgesic nephropathy is characterized by poor clinical symptoms. Abnormal urinary findings are rare. The disease is usually discovered if advanced renal damage has occurred with elevated serum creatinine, papillary necrosis, microhematuria and renal colics. There is abundant evidence, that abuse of phenacetin leads to analgesic nephropathy. Aspirin may have only an additive effect with phenacetin in causing renal damage. The primary medullary changes caused by phenacetin or one o f its metabolites are: Interstitial fibrosis, thickening of tubular basement membrane, loss of tubular epithelium and finally destruction of the loops of Henle. The consequence of these histological changes is a loss of urinary concentrating ability, one of the earliest findings in analgesic nephropathy. Inflammatory cell infiltration and involvement of the renal cortex with corresponding functional defects are secondary. Intravenous pyelography reveals in this stage of the disease symmetrically shrunken kidneys with a smooth wavy outline, whereby in contrast to the pyelonephritic changes the prtrusions correspond with the renal calyces. Papillary necrosis with the typical "halo shacow" in the pyelogramm rarely leads to the discovery of the disease.--Cessation of phenacetin consumption is usually associated with stabilization of renal funciton in patients with serum creatinine levels below 1.5 mg percent; with elevated serum creatinine there is a slow progression of the disease.--Analgesic nephropathy may be prevented by high fluid intake and avoidance of more than 150 g phenacetin per year respectively 0.5 g per day. Coffein, a constituent of many preparations, has a protective effect only with sufficient fluid intake.--The socio-economic importance of the analgesic nephropathy is given by the fact, that in the German Federal Republic 10 percent and in Australia even 20 percent of the patients requiring recurrent dialysis suffer from analgesic nephropathy. The following measures have been found to be effective in order to reduce phenacetin abuse: 1. Preparations containing phenacetin subject to prescription. 2. No advertising in newspapers and television. 3. Detailed information about kidney damaging effect of phenacetin on each packaging.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P Kramer. 1975-05-16. [Analgesic nephropathy].. https://pubmed.ncbi.nlm.nih.gov/1134426/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Sibling cases of Vici syndrome: sleep abnormalities and complications of renal tubular acidosis.

Vici syndrome is a rare congenital disorder characterized by albinism, agenesis of the corpus callosum, and developmental delays. Cardiac complications usually cause poor prognosis. We report sibling cases of Vici syndrome, and address complications of renal tubular acidosis. We also demonstrate the significance of serial examinations of brain natriuretic peptides, and discuss the possible early use of a beta-blocker to control cardiomyopathy. A sleep study including polysomnography indicated functional brainstem involvement, in which muscle atonia during non-rapid sleeping eye movements, and bursts of rapid eye movements increased. These findings provide new clues for medical care of patients with Vici syndrome.

Acidosis, Renal Tubular↗

Inadequate dietary intake but not renal tubular acidosis is associated with bone demineralization in primary biliary cirrhosis.

BACKGROUND: Metabolic bone disease associated with primary biliary cirrhosis (PBC) is inadequately characterized. Renal tubular acidosis (RTA) may lead to bone loss through chronic mobilization of skeletal calcium salts to buffer increased acid load. AIM: To evaluate the prevalence of RTA in PBC and establish the relationships among bone mineral density (BMD), renal function and nutritional status. METHODS: We enrolled 69 female patients with compensated PBC and 35 control patients with chronic hepatitis C. RTA was searched in all patients, and 24-h dietary recalls were collected at enrolment. BMD was measured by dual-energy X-ray absorptiometry at the femur neck, lumbar spine and radius ultradistalis sites. RESULTS: No patients received a diagnosis of RTA. BMD values (Z-scores) showed only little deviation from normal population with no difference between PBC and controls. Osteopoenic PBC patients (T-score < 1) showed significantly lower daily phosphorus intake [median: 672 (288-1374) vs. 921 (253-1923) mg/day; P = 0.037], with a trend towards lower caloric intake than their nonosteopoenic counterparts. CONCLUSIONS: Renal tubular acidosis is uncommon in compensated PBC. Cholestasis is not associated with an increased risk of bone demineralization. Inadequate dietary intake may be a preventable factor contributing to bone loss in PBC.

Acidosis, Renal Tubular↗

Distal RTA with nerve deafness: clinical spectrum and mutational analysis in five children.

Distal renal tubular acidosis (RTA) with nerve deafness is caused by mutations in the ATP6V1B1 gene causing defective function of the H+ -ATPase proton pump. We report five acidotic children (four males) from four unrelated families: blood pH 7.21-7.33, serum bicarbonate 10.8-14.7 mEq/l, minimum urinary pH 6.5-7.1 and fractional excretion of bicarbonate in the presence of normal bicarbonatemia 1.1-5.7%. Growth retardation and nephrocalcinosis, but not hypercalciuria, were common presenting manifestations. Hearing was normally preserved in one of the patients whose sister was severely deaf. One child was homozygous for a known mutation in exon 1: C>T (R31X). Three children were homozygous for a splicing mutation, intron 6 + 1G>A. The other patient was a compound heterozygote, having this mutation and a previously unreported mutation in exon 10: G>A (E330K). Our report shows that hearing loss is not always present in the syndrome of distal renal tubular acidosis with nerve deafness and the absence of hypercalciuria at diagnosis and describes a new mutation responsible for the disease in the ATP6V1B1 gene.

Acidosis, Renal Tubular↗