Renal cortical infarcts in sickle-cell trait.

Abstract

The renal complications of sickle-cell trait are hyposthenuria (Zarafonetis et al., 1954) and massive haematuria from renal papillary necrosis (Chapman et al., 1955; Akinkugbe, 1967). These and several other reports have shaken the view that sicklecell trait is a benign condition. Also, Raper (1952Raper ( , 1953 claimed that cicatricial obliteration of glomeruli, which he observed from histological examination of necropsy kidneys, was often associated with sickle-cell trait.Though several cases of haematuria from renal papillary necrosis have been documented in patients with sickle-cell trait, nothing has been written about renal cortical infarcts in these patients. After a few days in hospital he gave a history of having had good health until mid-August 1967, when he felt a dull pain of gradual onset in the low back and left loin. He attended another hospital for treatment. The pain disappeared within a week. Three days before the present admission he felt dizzy on standing upright and was breathless and had palpitations on exertion.Investigations.-The following were found on his admission: Hb 9.8 g./100 ml.; P.C.V. 33% ; sickling positive; Hb genotype A.S.; E.S.R. 79 mm. in the first hour; blood urea 62 mg./100 ml.; serum HCO3-21 mEq/l.; Cl-96 mEq/i.; Na+ 132 mEq/l., K+ 4.2 mEq/l. Antistreptolysin 0 titre, 100 Todd units; blood W.R.and Kahn test were negative; serum cholesterol was 233 mg./100 ml. Chest x-ray examination showed an enlarged heart with pulmonary oedema. E.C.G. was of left ventricular hypertrophy pattern. Urine microscopy and culture were normal. With control of left ventricular failure the blood urea fell to 30 mg./100 ml. Intravenous pyelography (I.V.P.) showed a non-functioning contracted left kidney; the right kidney was normal. Cystoscopy showed a very small left ureteric orifice. Retrograde pyelography was therefore not performed. Facilities for aortography were not available at that time. The 24-hour urinary catecholamines were normal.Operative Findings (Professor A. 0. Adesola).-On 26 October the left kidney was explored; it appeared to be of normal size. Three branches of the renal artery were identified, but the superior branch, which appeared to be the largest, was not pulsating. Nephrectomy was performed.Pathological Findings.-The resected kidney measured 8 by 4 by 2 cm. (see Fig.). The capsule stripped easily, revealing a smooth brownish-red surface with three wedge-shaped yellowish infarcted areas depressed for 2 to 3 mm. below the renal surface. One was at the upper pole and the others in the middle and lower zones. On sectioning, the renal vessels were seen to be filled with clotted blood. The cortex and medulla were clearly demarcated. Sections from various parts of the kidney showed large, small, and mediumsized vessels full of red cells with sickle appearances. Many glomeruli also showed plugging of glomerular capillaries with sickle cells. Some glomeruli were of normal size, while others were small and showed partial or total obliteration of the tufts. In some fields the glome...

The Influence of Indomethacin on Renal Haemodynamics in Sickle Cell Anaemia

“…Inulin and paminohippurate were determined as previously described (Statius van Eps et al, 1967), electrolytes by flame photometer IL 343 (Instrumentation Laboratories Inc., Lexington, MA, U.S.A.), creatinine and urea by Technicon Auto-Analyzer 11, method numbers 11 and 01 respectively (Technicon Instruments, Tarrytown, NY, U.S.A.), osmolality with a Fiske osmometer model 1 OSTM (Fiske Associates, Uxbridge, MA, U.S.A.). Plasma renin activity (Freedlander, Fyhrquist & Hollemans, 1974) and plasma aldosterone concentration (Pratt, Boonman, Woldring & Donker, 1978) were measured by radioimmunoassay. Mean arterial pressure was calculated as the sum of diastolic blood pressure plus one-third of pulse pressure.…”

The Perfusion Paradox and Vascular Instability in Sickle Cell Disease

“…During vasoocclusive crisis, entrapment of sickle erythrocytes may occur in the kidney not only in medullary regions, but also in the cortex. Cortical ischemia may be so severe as to cause cortical infarction (37,65,71,102). Acute occlusion of the renal artery with infarction of the involved kidney has also been described in sickle crisis (46).…”

Ketorolac-induced irreversible renal failure in sickle cell disease: a case report

“…Interstitial nephritis is an adverse reaction of ketorolac and other NSAIDs [6,25,34,35], although that diagnosis is unlikely in this case due to the mild inflammation and lack of improvement of renal function over time. Renal infarction in those with SCD and sickle cell trait has been described by others [39,40]. Therefore, we do not attribute the renal infarction that occurred in our patient to the ketorolac treatment she received.…”