Wednesday 26 June 2019

Lupine Publishers-Journal of Diabetes and Obesity




83 year-old Caucasian female with past medical history of hypertension, chronic kidney disease stage3-4 secondary to hypertensive nephrosclerosis with minimal proteinuria, hypokalemia, and Sjugrene syndrome without extra-glandular involvement. The patient was admitted to hospital because of urinary tract infection and edema of the lower extremities. She was treated with antibiotics, and diuretics for the edema. Her blood pressure was not optimum at this visit and spironolactone 25mg was added to her medication to control her BP, hypokalemia, and proteinuria. She was on amlodipine, frusemide, clonidine, Irbesartan, and potassium supplement. The treating nephrologist decided to try spironolactone for better control of high BP and hypokalemia and phased out the potassium supplementation. At this encounter her micro-albumin-creatinine ratio was 379.3mg/ gr, (normal value <29.9mg/gr creatinine). Physical examination was otherwise normal except bilateral leg edema, and high blood pressure (149/65mmHg). Her estimated glomerular filtration rate (EGFR) was 28ml/min).

She returned to the nephrology clinic after 2 weeks for bilateral lower extremities itch, burning and painful rash involving the buttocks, upper thighs and shins bilaterally as shown in the (Figures 1 & 2). The rash was palpable, purpuric nodules symmetrically distributed over the lower extremities. She was sending for dermatological opinion and skin biopsy of the rash. The biopsy was consistent with leukocytoclastic vasculitis. On further questioning the patient, she recalled that she had had a similar rash long time ago when she was placed on “aldactone” and the doctor had to stop the medication because of the rash, subsequently, the rash went away. This triggered discontinuation of the spironolactone and she was treated with prednisone and topical steroids by the dermatologist. The current rash faded away in 3-4 weeks; however, she was still on 5mg of prednisone when she was last seen in the clinic.Spironolactone is potassium sparing mineral ocorticoid receptor antagonist (MRA) which acts on the distal tubules and collecting ducts of the kidneys and antagonizing the effect of aldosterone, thereby causing inhibition of sodium and chloride re absorption, and potassium secretion in the distal tubules. The bioavailability of spironolactone is 73%, and it is >90% protein-bound. The drug is extensively metabolized in the liver and excreted by renal (47- 57%), bile and eventually fecal route (35-41%). The elimination half-life of the drug ranges from 1.4 to 15- hours depending on the type of metabolites. It is indicated for heart failure with reduced ejection fraction, hypertension especially when associated with hyperaldosteronism, hypokalemia, precocious puberty, hirsutism and female virilization syndrome. The American geriatric association (AGS) recommends that the drug should be avoided in patients >65 years old when creatinine clearance <30ml/minute due to increased potassium levels associated with the medication [1]. Spironolactone has also been used for liver cirrhosis with as cites and diabetic nephropathy with proteinuria. It can be added to patients with metabolic alkalosis with hypokalemia due to diuretic use.To know more click on below link.

 
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