Analgesic nephropathy

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Classification according to ICD-10
N14.0 Analgesic nephropathy
ICD-10 online (WHO version 2019)

The classic analgesic nephropathy (also called phenacetin kidney ) is a chronic tubulo-interstitial nephropathy that is caused by long-term abuse of mixed analgesics . Phenacetin plays the dominant role among its components . In addition, were paracetamol , acetylsalicylic acid (ASA) and other NSAIDs (including COX-2 inhibitors cause considered).

Epidemiology

Patients with heavy use of mixed analgesics with phenacetin are approximately 20 times more likely to develop end-stage renal disease . A two to three-fold increased risk has been reported for the use of paracetamol-containing mixed analgesics, but not for paracetamol or ASA alone.

Analgesic nephropathy was the cause of about 3 to 10% of all cases of chronic kidney failure . It was particularly common in Australia, Belgium, Switzerland, Sweden, the GDR, Eastern Europe and the southeastern United States. In Germany, it is estimated that the proportion of patients with analgesic nephropathy before the phenacetin ban (BRD 1986, GDR 1990) among patients requiring dialysis was four to nine percent. Women are three to five times more likely to be affected than men.

Michael J. Mihatsch reported in 2006 that 20 years after the phenacetin ban (despite continued use of paracetamol-containing mixed analgesics, for example in the combination preparation Togal ), the analgesic nephropathy had almost disappeared in the autopsy material at the University of Basel . This corresponds to the observations made by nephrologists in western countries.

etiology

Phenacetin and its metabolite paracetamol as well as other nonsteroidal anti-inflammatory drugs block the synthesis of prostaglandin-E2 , which has a vasodilatory (vasodilating) effect. This leads to circulatory disorders with capillary sclerosis and subsequent necrosis of the renal papillae . Phenacetin can be assumed to have a direct toxic effect on the renal papillae.

The tubulointerstitial nephritis of analgesic nephropathy primarily damages the tubules and not the glomeruli . Dose-dependent tubular cell necrosis are described . Nevertheless, the glomerular filtration rate decreases until dialysis is required in terminal kidney failure. It may, for analgesics syndrome come.

clinic

In the early stages, the clinical picture is often clinically silent. Sometimes patients complain of headaches . First there is a dirty, gray-brownish discoloration of the skin (skin color). In most cases there is also anemia , which is initially caused by blood loss via the gastrointestinal tract as well as by hemolysis and the formation of methemoglobin and sulfhemoglobin . A renal anemia is usually found later. The loss of necrotic papillae parts leads to colic with hematuria and urine congestion in the form of hydronephrosis or pyonephrosis ( purulent hydronephrosis ). Secondary pyelonephritis often dominates . The analgesic nephropathy can lead to terminal chronic kidney failure.

The analgesic syndrome in the phenacetin kidney includes progeria , underweight , cyanosis , arteriosclerosis , arterial hypertension , gastritis , gastric ulcer , renal pelvic inflammation , renal pelvic tumors , ureteral tumors and anemia .

The late complication of phenacetin abuse is the increased risk of urothelial carcinoma ; about 10 percent of patients with analgesic nephropathy develop a malignant urinary tract tumor .

diagnosis

In terms of history , a total consumption of more than 1000 g phenacetin is groundbreaking. If it is suspected that the patient is hiding a phenacetin abuse, the breakdown product N-acetyl-paraaminophenol (NAPAP) can be determined in the urine (Herold).

A lower limit for the development of analgesic nephropathy appears to be one gram of phenacetin daily for one to three years, or a total of one kilogram of phenacetin in combination with other analgesics.

In the advanced stages of sonography and computed tomography (if possible without contrast agent ), smaller kidneys with irregular contours, scarred indentations of the renal cortex over the medullary cones and - even at an early stage - calcification of the papillae and papillary necrosis can be found . With the improved multidetector CT urography (MDCTU), a so-called all-in-one examination is possible, in which an empty abdomen, a urogram and ultrasound diagnostics can be dispensed with.

The urine test shows leukocyturia , usually without bacteriuria (unless complicating pyelonephritis is present), possibly erythrocyturia, and slight proteinuria (tubular proteinuria).

Differential diagnosis

In terms of differential diagnosis , other chronic tubulo-interstitial nephritis should be considered, as well as diabetic or obstructive nephropathy (chronic postrenal kidney failure ) of other origins , urogenital tuberculosis or sickle cell anemia .

Analgesic nephropathy is caused by toxins that are foreign to the body. The uremia is by endogenous uremic toxins ( Urämiegifte ) and nephrotoxins caused.

Therapy and prognosis

Omitting the triggering noxious agent (especially phenacetin) is the crucial step in therapy. If this succeeds before severe renal insufficiency occurs, the disease process comes to a standstill. In severe cases, kidney replacement therapy should be considered. Treatment of secondary pyelonephritis and urinary obstruction is important. The alternatives to drug therapy for renal failure are limited.

See also

Individual evidence

  1. ↑ The Merck Manual , 20th Edition, Merck, Sharp & Dohme , Kenilworth (New Jersey) 2018, ISBN 978-0-911910-42-1 , p. 2164.
  2. ^ Ulrich Kuhlmann, Joachim Böhler, Friedrich C. Luft , Mark Dominik Alscher , Ulrich Kunzendorf (eds.): Nephrology , 6th edition, Georg Thieme Verlag , Stuttgart, New York 2015, ISBN 978-3-13-700206-2 , Pp. 519-523.
  3. ↑ Willibald Pschyrembel: Clinical Dictionary , 267th edition, de Gruyter Verlag, Berlin, Boston 2017, ISBN 978-3-11-049497-6 , p. 80.
  4. ^ Harrison's internal medicine , 19th edition, Georg Thieme Verlag , Stuttgart 2016, ISBN 978-3-88624-560-4 , p. 2290 f.
  5. ↑ Michael J. Mihatsch , Bettina Khanlari and Felix Brunner: Obituary to analgesic nephropathy - an autopsy study. In: Nephrology Dialysis Transplantation 2006; 21, pp. 3139-3145.
  6. ↑ Paul Michielsen. In memoriam analgesic nephropathy (circa 1972–2006). In: Nephrology Dialysis Transplantation 2007; 22, pp. 999-1001.
  7. ↑ Peter Reuter: Springer Clinical Dictionary, 1st edition, Springer-Verlag, Heidelberg 2007, ISBN 978-3-540-34601-2 , p. 70.
  8. ↑ Gerd Herold : Internal Medicine 2020, self-published, Cologne 2019, ISBN 978-3-9814660-9-6 , p. 625 f.
  9. ↑ Maxim Zetkin , Herbert Schaldach (Ed.): Lexikon der Medizin , 16th edition, Ullstein Medical, Wiesbaden 1999, ISBN 978-3-86126-126-1 , p. 80.
  10. ↑ Helmut Geiger, Dietger Jonas, Tomas Lenz, Wolfgang Kramer (eds.): Kidney Diseases , Schattauer , Stuttgart, New York 2003, ISBN 3-7945-2177-3 , pp. 102-104.
  11. ↑ Maxim Zetkin , Herbert Schaldach (Ed.): Lexikon der Medizin , 16th edition, Ullstein Medical, Wiesbaden 1999, ISBN 978-3-86126-126-1 , p. 80.
  12. ^ Lexicon Medicine , 4th edition, Naumann & Göbel Verlag, Cologne no year [2005], ISBN 978-3-625-10768-2 , p. 63.
  13. ^ Ulrich Kuhlmann, Joachim Böhler, Friedrich C. Luft , Mark Dominik Alscher , Ulrich Kunzendorf (eds.): Nephrology , 6th edition, Georg Thieme Verlag , Stuttgart, New York 2015, ISBN 978-3-13-700206-2 , Pp. 61 and 542.