A 55-year-old man is seen during a routine evaluation. He was diagnosed with type 2 diabetes mellitus 15 years ago. He also has hypertension and a 1-year history of right knee osteoarthritis that is well controlled with maximal-dose ibuprofen. His other medications are losartan, metformin, and pravastatin.
On physical examination, temperature is 37.2°C (98.9°F), blood pressure is 146/92 mm Hg, pulse rate is 70/min, and respiration rate is 14/min. Cardiopulmonary examination is normal. There is bilateral lower-extremity edema to the mid shin.
| Glucose (nonfasting) |
230 mg/dL (12.8 mmol/L) |
| Sodium |
142 meq/L (142 mmol/L) |
| Potassium |
5.9 meq/L (5.9 mmol/L) |
| Chloride |
108 meq/L (108 mmol/L) |
| Bicarbonate |
18 meq/L (18 mmol/L) |
| Serum creatinine |
2.5 mg/dL (221 µmol/L) |
| Urine protein-creatinine ratio |
0.46 mg/mg |
| Urinalysis |
Specific gravity 1.015; 3+ protein; 2+ glucose; no casts |
Discontinuation of ibuprofen and initiation of furosemide are the most appropriate next steps in the initial management of this patient's chronic kidney disease. This patient's long-standing history of diabetes mellitus, hypertension, proteinuria, and elevated serum creatinine level are consistent with diabetic nephropathy. Aggressive blood pressure control, particularly with pharmacologic modulators of the renin-angiotensin-aldosterone system, would help to slow the progression of this patient's disease but will likely worsen his hyperkalemia.
Until the glomerular filtration rate decreases to less than 15 mL/min/1.73 m2, chronic kidney disease usually does not cause hyperkalemia without other mitigating factors. These factors include use of medications that interfere with the renin-angiotensin-aldosterone system and NSAIDs. Use of the NSAID ibuprofen is most likely contributing to this patient's hyperkalemia and reduced glomerular filtration rate and should be discontinued.
However, discontinuing ibuprofen alone would most likely not help to lower this patient's blood pressure, control volume overload, or fully correct his hyperkalemia; the addition of a loop diuretic is therefore warranted. If needed, additional interventions to help decrease the risk of hyperkalemia include adherence to a low-potassium diet and use of sodium bicarbonate.
Thiazide diuretics are largely ineffective in individuals with an estimated glomerular filtration rate below 30 mL/min/1.73 m2.
The addition of losartan would worsen this patient's hyperkalemia and would not be recommended.
Spironolactone has been shown to further decrease urine protein excretion when added to either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in patients with diabetic nephropathy. However, this agent impairs kidney potassium excretion and also would further exacerbate this patient's hyperkalemia.
Key Point
- Discontinuation of medications that interfere with the renin-angiotensin-aldosterone system, including NSAIDs and, if needed, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, is warranted to help correct significant hyperkalemia in the setting of chronic kidney disease.
