Renal bilateral

Despite their clear benefits, ACE inhibitors are still underutilized in HF. One reason is undue concern or confusion regarding absolute versus relative contraindications for their use. Absolute contraindications include a history of angioedema, bilateral renal artery stenosis, and pregnancy. Relative contraindications include unilateral renal artery stenosis, renal insufficiency, hypotension, hyperkalemia, and cough. Relative contraindications provide a warning that close monitoring is required, but they do not necessarily preclude their use. 

Acute renal failure is a rare but serious side effect of ACE inhibitors preexisting kidney disease increases the risk. Bilateral renal artery stenosis or unilateral stenosis of a solitary functioning kidney renders patients dependent on the vasoconstrictive effect of angiotensin II on efferent arterioles, making these patients particularly susceptible to acute renal failure. 

ACE inhibitors, ARBs, and direct renin inhibitors are contraindicated in sexually active girls because of potential teratogenic effect and in those who might have bilateral renal artery stenosis or unilateral stenosis in a solitary kidney. 

Isolated renal hypoperfusion Bilateral renal artery stenosis (unilateral renal artery stenosis in solitary kidney) Emboli Cholesterol Thrombotic Medications Cyclosporine Angiotensin-converting enzyme inhibitors Nonsteroidal antiinflammatory drugs Radiocontrast media... 

Left ventricular dysfunction Post-myocardial infarction Non-diabetic nephropathy Type 1 diabetic nephropathy Type 2 diabetes mellitus Proteinuria Hyperkalaemia Bilateral renal artery stenosis disease... 

ARBs Type 2 diabetic nephropathy Type 2 diabetic microalbuminuria Proteinuria Left ventricular hypertrophy ACE-I cough or intolerance Pregnancy Hyperkalaemia Bilateral renal artery stenosis ... 

Contraindications Bilateral renal artery stenosis, hyperaldosteronism... 

Contraindications Bilateral renal artery stenosis, biliary cirrhosis or obstruction, primary hyperaldosteronism, severe hepatic insufficiency... 

Contraindications Bilateral renal artery stenosis, history of angioedema from previous treafmenf wifh ACE inhibitors... 

Severe hypotension can occur after initial doses of any ACE inhibitor in patients who are hypovolemic as a result of diuretics, salt restriction, or gastrointestinal fluid loss. Other adverse effects common to all ACE inhibitors include acute renal failure (particularly in patients with bilateral renal artery stenosis or stenosis of the renal artery of a solitary kidney), hyperkalemia, dry cough sometimes accompanied by wheezing, and angioedema. Hyperkalemia is more likely to occur in patients with renal insufficiency or diabetes. Bradykinin and substance P seem to be responsible for the cough and angioedema seen with ACE inhibition. 

A group of 60 female Wistar rats, 15 weeks of age, received two subcutaneous injections of 120 mg/kg bw 1,2-dimethylhydrazine (calculated as base) at 10-day intervals. Twenty-three animals were killed 30 weeks after the first injection. Thirteen of 23 animals exhibited tumours of the colon and one a tumour of the small intestine. Twenty-one (91%) of 23 rats developed renal tumours in 10 rats, they were bilateral and in six rats, there was more than one tumour per affected kidney. All neoplasms were diagnosed as mesenchymal kidney tumours (Sunter Senior, 1983). 

A group of 40 weanling outbred female Wistar rats received a single subcutaneous injection of 200 mg/kg bw 1,2-dimethylhydrazine. Four rats died within four days after the injection. Twenty-five of 36 rats that survived for more than four days and were killed within one year after 1,2-dimethylhydrazine administration developed renal tumours, nine of them bilateral. Pulmonary metastases were foimd in one animal. Twenty-five (73%) of 34 tumours examined histologically were diagnosed as nephroblastoma-like tumours similar to human Wilms tumour, three were mesenchymal tumours, three were adenomas, two were adenocarcinomas and one was unclassifiable (Sadrudin et al., 1985). 

A 60-year-old woman took dexamethasone 4 mg 8-hourly for dyspnea due to a precursor T lymphoblastic lymphoma-leukemia with bilateral pleural effusions and a large mass in the anterior mediastinum (130). She developed acute renal insufficiency and laboratory evidence of the metabolic effects of massive cytolysis. She received vigorous hydration, a diuretic, allopuri-nol, and hemodialysis. She recovered within 2 weeks and then underwent six courses of CHOP chemotherapy. The mediastinal mass regressed completely. She remained asymptomatic until she developed full-blown acute lymphoblastic leukemia, which was resistant to treatment. 

It is well recognized that antithyroid drugs, and especially propylthiouracil, can be associated with development of anti-neutrophil cytoplasmic antibody (ANCA)-positive vasculitis, often manifesting as renal disease. Atypical presentations, with pyoderma gangrenosum (49) and progressive bilateral sensorineural hearing loss (50), have been described in separate case reports of subjects taking propylthiouracil. 

A 78-year-old man became short of breath. He had been taking rosiglitazone 8 mg/day for 6 months. He had renal insufficiency, atrial fibrillation, hypertension, and congestive heart failure, with pitting edema and bilateral pleural effusions. He was refractory to intravenous furosemide and metolazone. Withdrawal of rosiglitazone and administration of bumetanide gave a net fluid output of 9.5 litres and the edema resolved. 

A 64-year-old man with type II diabetes, hypertension, and bilateral renal artery stenosis presented with confusion and dysarthria related to profound hypoglycemia (2.2 mmol/1). He was taking naproxen 500 mg bd, ramipril 2.5 mg/day, glibenclamide 2.5 mg bd, metformin 850 mg bd, a thiazide diuretic, terazosin, ranitidine, paracetamol, and codeine. His plasma creatinine concentration, previously 185 pmol/1, was 362 pmol/1 and it fell to 210 imol/l after the withdrawal of ramipril and naproxen. 

In animal models of acute renal failure induced in rats by bilateral nephrectomy and bilateral ureteral ligation, TAC increased, probably due to the accumulation of urate and uremic toxins with scavenging capacity, such as hyppurate (B19, S9). TAC of blood plasma was reduced in a rat endotoxic shock model (rats given i.p. 5 mg/kg lipopolysaccharide) (Cl6). 

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