Mr DJ is a 26-year-old student, a male, who was diagnosed with SCA in childhood. He was adherent to his routine medications and regular to follow up. He presented with 2 weeks history of oliguria and passage of frothy urine. This was preceded by swelling of the leg and face a week prior to presentation. This was associated with anorexia, weakness of the body, early satiety, abdominal fullness, and nausea. 
There was no fever, vomiting, jaundice, or change in bowel habit. He had cough productive of frothy sputum but no haemoptysis or chest pain; however, he had dyspnoea, orthopnoea, and paroxysmal nocturnal dyspnoea.
He has had few bone pain crises, and these were usually treated with rehydration, opiate analgesic, antimalarial, and/or antibiotics. He was transfused on 2 occasions as a result of the crises and twice during the course of this illness. He is not a known hypertensive or diabetic and no family history of same or kidney disease. There no positive history of use of herbs, mercury, alcohol, or tobacco. He is the only sickler in a family of 3 siblings; both parents are alive and well. 
He was conscious but in respiratory distress. He had anasarca, pallor, and asterixis but no cyanosis. The pulse was 108 beats/minute, full volume, and regular, the blood pressure was 160/90 mmHg, the praecordium was hyperactive, and apex beat was displaced and heaving. The heart sound heard were S1, S2, and S3 gallop with pansystolic murmur maximal at the apex. 
He had bilateral basal fine crepitations, distended abdomen with firm smooth hepatomegaly and ascites. He was conscious and had no asterixis. 
He was admitted as a case of sickle cell cardiomyopathy in congestive cardiac failure, with sickle cell nephropathy as a differential diagnosis. 
 Investigations results revealed that urinalysis showed proteinuria 3+. PCV was 14%, blood film hypochromia, polychromasia, anisocytosis, and fragmented cells. The total and differential white blood cell count was normal, and ESR was 94 mm/hr. The serum sodium was 132 mmol/L, potassium was 4.1 mmol/L, bicarbonate was 13 mmol/L, creatinine was 645 mumol/L, urea was 35 mmol/L, calcium was 2.3 mmol/L, total protein was 59 mg/dL, albumin was 28 mg/dL, total cholesterol was 5.2 mmol/L, LDL was 3.2 mmol/L, and HDL was 1.1 mmol/L.
The abdominal ultrasound showed bilateral shrunken kidneys, hepatomegaly, and ascites. Other viscera were normal. 
Chest X-ray showed marked cardiomegaly, pulmonary oedema as abnormality.
Echocardiography revealed marked 4-chamber dilatation and biventricular failure.
The diagnosis was then changed to sickle cell nephropathy with congestive cardiac failure. He was comanaged with the cardiologist.
He was advised on low salt diet, care on protein intake, and was commenced on tabs Ramipril, hydrochlorothiazide, frusemide, digoxin, erythropoietin, folic acid, proguanil, vasoprine, and erythropoietin. He was also on twice weekly haemodialysis. He was transfused with 2 units of packed red blood cell.
The haemodialysis including ultrafiltration and medication was regular; however, the breathlessness and ascites persisted. Weekly therapeutic abdominal paracentesis for symptomatic relief was then instituted while awaiting result of other investigations.
Results of further investigations revealed sterile exudative ascitic fluid. Chest CT scan revealed enlarged heart, mild pericardial effusion, and prominent main pulmonary artery. Abdominal CT scan revealed bilateral small kidneys, gross ascites, hepatomegaly, cholelithiasis, dilatation of the portal vein, and prominent collaterals seen at the porta hepatis. BACTEC blood culture was positive for tuberculosis. Other investigations were consistent with previous results as documented above.
The managing team then was expanded and included nephrologists, infectious disease physician, cardiologist, gastroenterologist, and haematologist.
The frequency of haemodialysis was increased to daily, antituberculous therapy was commenced, and tabs Sildenafil were added to the medications above. He improved remarkably within 2 weeks of these regimens. 
The patient improved progressively, and 4 weeks later he had a successful and live-related kidney transplant. There was no operative or immediate postoperative complication. He is 1-year posttransplant, there was complication, and he has remained stable clinically, biochemically, and haematologically. His present blood pressure was 120/70 mmHg, PCV was 25%, sodium was 137 mmol/L, potassium was 4.1 mmol/L, Serum creatinine was 96 umol/L, serum urea was 5.3 mmol/L, and tacrolimus level was 4.8 ng/L.