We questioned 180 patients with end-stage renal disease on maintenance haemodialysis, chronic ambulatory peritoneal dialysis and those who had undergone renal transplantation at the Department of Nephrology, General Hospital, Kuala Lumpur. Twelve patients (6.7%) had consumed excessive quantities ofanalgesics prior to the institution of long-term dialysis or transplantation. Primary renal disease was considered to be analgesic nephropathy in seven patients (3.9%); in five patients (2.8%), analgesic abuse could have been a contributory factor to end-stage renal failure. Analgesic nephropathy is hence an uncommon cause of end-stage renal disease in Malaysia. However, it is important to be aware of the problem and to institute preventive measures as the cost of treatment for end-stage renal disease is prohibitive.
The risk of renal papillary necrosis and renal dysfunction due to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) is unknown. In a prospective study of 259 heavy analgesic users seen in a general medical hospital over an 11-year-period beginning in January 1982, 69 new cases of analgesic nephropathy with renal papillary necrosis were confirmed by intravenous urogram (26.6%), ultrasonography (30.4%), and/or computed tomography (43%). Twenty-nine of these patients (42%) had consumed excessive quantities of NSAIDs alone; an additional nine patients (13%) had consumed NSAIDs predominantly in combinations with paracetamol, aspirin, phenacetin, caffeine, and/or traditional herbal medications. Of those patients who consumed NSAIDs alone, 17 had consumed only a single type of NSAID and the remaining 12 had consumed multiple types of NSAIDs. The amount of NSAIDs administered ranged from 1,000 to 26,600 capsules or tablets over a 2- to 25-year period. Renal impairment (serum creatinine, 126 to 778 mumol/L) was noted in 26 of these 38 patients (64.8%). The reasons given for consuming NSAIDs include gouty arthritis (18 patients), osteoarthritis (seven patients), rheumatoid arthritis (six patients), chronic headache (three patients), gouty arthritis plus chronic headache (three patients), and chronic backache (one patient). All patients were prescribed these drugs and were followed medically. The occurrence of analgesic nephropathy was predominantly in males (male to female ratio, 1.9:1). Most of the patients did not have the characteristic psychological profile attributed previously to analgesic abuse nephropathy. Associated addictive habits, such as the use of psychotropic drugs and sleeping tablets, purgative abuse, and alcoholism, were absent.(ABSTRACT TRUNCATED AT 250 WORDS)
Seven cases of analgesic nephropathy due to excessive ingestion of paracetamol are reported. None of these patients had been taking any other analgesic. All had radiological features of papillary necrosis. With the increasing use of paracetamol as a mild analgesic it is necessary to be aware of the possibility that paracetamol may induce analgesic nephropathy.
180 patients with end-stage renal disease (ESRD) on maintenance dialysis and those who had undergone renal transplantation were questioned retrospectively. 14 patients had consumed excessive quantities of analgesics (greater than 1 kg) prior to the institution of long-term dialysis or transplantation. Sonographic examination done on these patients indicated that 7 had renal papillary necrosis (RPN). The sonographic features were renal papillary calcifications surrounding the central sinus in a complete or incomplete garland pattern. In 5 of these patients RPN is attibutable to the excessive consumption of paracetamol. We have earlier reported 10 cases of RPN due to excessive consumption of paracetamol. Thus 15 cases of RPN attributable to paracetamol consumption (1.0-15.3 kg over a period ranging from 3 to 23 years) have been documented. It is concluded that paracetamol may assume an increasingly important role in the causation of analgesic nephropathy (AN) and ESRD.
The pattern of analgesic use, abuse and incidence of analgesic-associated nephropathy in 79 patients with chronic headache was studied. Sixty-eight of these patients had migraine. Most patients had consumed a combination of analgesics (81%) while 19% had taken single analgesics for their headache. Nonsteroidal anti-inflammatory drugs were the most commonly used analgesics (96.2%) followed by paracetamol (70.9%) and aspirin, phenacetin and caffeine compounds (5.1%). Mefenamic acid was the commonest nonsteroidal anti-inflammatory drug consumed (97.4%). Analgesic abuse which was defined as a minimum total of 1 kg of analgesics such as paracetamol or aspirin, phenacetin and caffeine compounds or 400 capsules/tablets of nonsteroidal anti-inflammatory drugs was noted in 65 patients. Nonsteroidal anti-inflammatory drugs were the most commonly abused analgesics (89.2%) followed by paracetamol (38.5%). Forty-five of the 65 analgesic abusers had an intravenous urogram or ultrasound performed and renal papillary necrosis was documented in one patient. Three (4.6%) of the analgesic abusers had mildly raised serum creatinine levels. Mild proteinuria of less than 1 gm/litre was present in 27.7% of abusers. In conclusion, although analgesic use and abuse is common in patients with chronic headache, the short term incidence of analgesic-associated nephropathy (2.2%) and renal impairment (4.6%) was low. Prolonged observations will be necessary to ascertain the safety of these drugs for long term use.
The aim of the present study was to investigate the effectiveness of transforming growth factor (TGF)-beta1 antisense oligodeoxynucleotides (ODN) in ameliorating deteriorated kidney function in rats with puromycin-induced chronic renal failure (CRF).