Papillary infarcts, demonstrable radiographically in 50% of patients with sickle trait, lead to an increased risk of bacterial infection in the scarred kidney tissues and functional tubule abnormalities. Other complications include end stage renal disease (ESRD), medullary carcinoma, nephritic syndrome due to concurrent HPV B19 infection (this infection can cause benign self-limiting red cell aplasia). Risk Factors
Genetic
When looking at SCN, the main contributors leading to either a decrease or increase in CKD progression are the type of hemoglobin inheritance, myosin heavy chain 9, and apolipoprotein L1 genes. In those with the HbSS or HbSβ0 (no normal hemoglobin), they exhibit more severe forms of renal dysfunction at a high occurrence rate compared to those with HbSS or HbSβ+ (reduced number of normal hemoglobin). This ties in with the fetal hemoglobin levels (HbF) in that HbF levels are directly proportional to renal protection, and it has been found that in those with HbSS, a greater than 20% elevation in HbF led to no significant loss in renal function. Alpha-thalassemia has also been found to decrease HbS levels where the co-inheritance of alpha gene deletions reduce red blood cells and hemolysis. This inheritance has been shown to protect against hyposthenuria but the effect on other symptoms are unknown. Specifically in the African American population, the inheritance of an S trait and/or a C trait increases the risk of developing ESRD. For myosin heavy chain 9, and apolipoprotein L1, polymorphisms in these genes can contribute to worsening proteinuria but are not specific towards SCD.
When predicting CKD progression, old age can be a contributor since there is an increase in renal injury and a  decrease in GFR in those over 30 years old. Also albuminuria, GFR, and lactic hydrogenase are used in determining CKD progression. The use of cystatin C may not be clear since while it increases when GFR declines, it has been shown that some people with SCN have similar levels to a healthy individual. Treatment
Lifestyle
Management of sickle nephropathy is not separate from that of overall patient management. Three-year graft and patient survival in kidney transplant recipients with sickle nephropathy is lower when compared to those with other causes of end-stage kidney disease.Certain medications should be avoided because of potential damage to the kidneys or can precipitate secondary complications. Nonsteroidal anti-inflammatory drugs (ibuprofen, naproxen) should be avoided because of the decrease in renal blood flow causing a decrease in GFR as well as causing hemodynamic injury from glomerular hypertension.For hematuria, if mild then bed rest and hydration is sufficient to prevent the breakage of clots and to maintain a healthy blood volume, and possibly antibiotics or analgesics if necessary. If severe, then it is recommended to do an ultrasound to see if there is a complication such as renal infarcts or papillary necrosis.