non - steroidal anti - inflammatory drugs ( nsaids ) are one of the most commonly prescribed drugs and their nephrotoxic effects are well known . reports of renal dysfunction have been documented mostly in volume decompensated patients and are favored by various drug interactions . we would like to report a case of diclofenac induced acute renal failure which was favored by the presence of co - morbid conditions namely , hypertension , falling renal function due to aging and drug interaction in a already volume decompensated patient . a 69 year old male patient was a known case of hypertension and receiving tablet atenolol 25 mg once a day since 3 years . he was diagnosed with spindle cell carcinoma on left thigh and was operated for it . before surgery , he was given tablet furesemide 40 mg once a day and his anti - hypertensive drug was continued . on discharge after surgery , he was asked to continue his antihypertensive therapy with tablet atenolol 25 mg once a day and was also prescribed tablet ranitidine 150 mg twice a day , a combination of diclofenac 50 mg with serratiopeptidase 10 mg thrice a day and another combination of ampicillin 250 mg and cloxacillin 250 mg thrice a day for a total duration of 7 days . after 7 days , he visited outpatient department with complaints of swelling over legs and decreased frequency of micturition . on examination , he had no pallor , icterus , lymphadenopathy or clubbing but he had pedal edema . his respiratory , cardiovascular and central nervous systems were within normal limits . on investigation , it was found that his plasma creatinine and urea were raised to 9.4 mg / dl and 99 mg / dl respectively . among the electrolytes , plasma potassium and sodium were 4.9 meq / l and 133 meq / l , respectively . these values of these tests when done 4 days prior to surgery were creatinine 1 mg / dl , urea of 17 mg / dl , potassium 4.6 meq / l and sodium 141 meq / l . urine proteins were within normal range with total protein 6.8 g / dl ( normal 6.0 - 8.3 g / dl ) urine albumin 3.47 g / dl ( normal 3.2 - 5.0 g / dl ) and urine globulin 3.34 g / dl ( normal 3.2 - 5.0 g / dl ) . meq / l ) and so the osmality to 34.2 meq / l ( normal values 100 - 260 his diclofenac was stopped and his investigations were repeated the following day , on day 5 , day 10 and after 1 month . his plasma creatinine and urea levels did nt show significant change on the following day but on day 5 the values started to drop towards normality with plasma creatinine 3.2 mg / dl , potassium 3.6 meq / l and sodium 137 meq / l . his pedal edema was also subsiding showing clinical improvement . on subsequent visit , on day 10 , his creatinine level further came down to 1.5 mg / dl , urea to 21 mg / dl , potassium 3.2 meq / l and sodium 140 meq / l . after one month , all the values returned within the normal range with creatinine 1.5 mg / dl and urea 16 mg / dl . non - steroidal anti - inflammatory drugs alter renal functions through their effects on renal prostaglandins leading to reversible renal ischemia . although nsaids related hypertension , salt and water retention , edema and hyperkalemia are highly infrequent but they remain a concern in patient who are at risk and can develop acute renal failure . prostaglandins do not play a physiologic role in maintaining renal blood flow in normal subjects ; but it plays a role in maintaining glomerular filtration rate ( gfr ) . in intravascular depleted states , renal plasma flow is maintained by a balanced between the vasoconstrictor influence of the renin angiotensin system and the vasodilatory effects of prostaglandins . in fluid depleted states , prostacyclin ( pgi2 ) mostly affects renal homeostatic mechanisms . pge2 and pgd2 cause dilatation of the renal vascular bed along with the lowering of renal vascular resistance . thus , it enhances renal perfusion with redistribution of blood flow from the renal cortex to nephrons in the juxta - medullary region . when the production of prostaglandins is blocked due to nsaids , it may lead to hyperkalemia , peripheral edema , increased blood pressure , weight gain and acute renal failure . in this case , the patient had no pre - existing renal disease but he was a known case of hypertension and received diuretic therapy prior to diclofenac admistration . age - related decline in renal blood flow in hypertensive person and volume depletion due to diuretics are further worsened by nsaids . this was clinically evident in our case as this patient belonged to the geriatric population so he was more susceptible to nephrotoxic drugs with his ageing kidneys . on presentation , his blood pressure was within normal range but he had marked pedal edema and decreased frequency of micturition . he also had low urine output , low sodium excretion and low urinary osmolality which signifies kidney 's decreased ability to concentrate urine . in the above setting , course with nsaids therapy i.e. , tablet diclofenac 50 mg three times a day ( 150 mg / day ) was sufficient to precipitate acute renal failure as this dose appears to impair the renal blood flow and glomerular filtration rate . diclofenac has antagonizing effect on atenolol which decreased its antihypertensive effect which further precipitates arf . thus , the hemodynamically mediated acute renal failure caused by nsaids was further exacerbated with interaction with anti - hypertensive drug . according to naranjo adverse drug reaction probability scale , hemodynamically - medicated acute renal failure due to nsaids in volume depleted patients is reversible and is mostly related to the dose and duration of exposure . in our case , patient 's plasma creatinine and urea started to decline after 7 days of drug discontinuation and his pedal edema subsided subsequently with improvement in urine output . within one month , on subsequent visit to outpatient department his investigation came within the normal range . in the above condition , either the nsaids ( nonselective and coxibs ) should have been given in lower doses as much as possible without re - titrating the anti - hypertensive drug dosage or adequate hydration of the patient should be maintained prior to initiation of nsaids therapy along with restriction of the dietary salt .
non - steroidal anti - inflammatory drugs ( nsaids ) are one of the most commonly prescribed drugs in post - operative period worldwide . their nephrotoxic effects are documented and accounts for around 15.5% of all cases of drug induced renal failure . 
 acute renal failure following nsaids usage are reported in volume depleted patients which is further precipitated by co - morbid conditions like hypertension and various drug interactions that increase plasma level of nsaids and worsens the condition . 
 this highlights the importance of hydration in post - operative period as well as assessment of co - morbid conditions before administration of nsaids to prevent acute renal failure .