Introduction: When sickled erythrocytes are present in the renal medulla, it causes ischemia, microinfarcts, and papillary necrosis in the kidneys. This condition is known as sickle cell nephropathy (SCN), which is the renal manifestation of sickle cell disease (SCD). Clinically presenting as increased GFR as a result of localised prostaglandin production and enhanced nitric oxide synthase in response to hypoxia, glomerular hyper filtration is the initial sign of SCN. This leads to an increase in renal blood flow and albuminuria 2. Proteinuria types 1 and 4 affect 20–30% of SCD patients. Material and Methods: We also measured height and weight using anthropometric techniques. The individuals’ shoes and top clothing were taken off before these measurements were taken. Every subject’s weight was recorded using digital weighing equipment, which was calibrated as needed and had its accuracy confirmed on a regular basis, to the nearest 0.1 kg. Using a portable stadiometer, the standing height was measured to the closest 1 cm. Weight (in kilogrammes) divided by height (in metres squared) was used to calculate BMI (kg/m2). Using a suitable blood pressure cuff size for the child’s upper arm and a relaxed forearm on the examination table, the resting Systolic blood pressure (SBP) was measured. Results: Similar to earlier studies, we discovered 5.83% of AKI patients in our investigation. According to Baddam S et al., 17% of vaso-occlusive pain crises had an AKI3 connection. Vasoocclusive pain crises were a frequent side effect in kids with SCA and a known risk factor for AKI, with 2.5–17% of kids admitted to the hospital due to a VOC going on to develop AKI136–38. Acute infection (malaria and sepsis), hypovolemia (insensible loss due to fever, reduced intake, diarrhoea, and vomiting), and the use of NSAIDs to manage Vaso-occlusive crises are recognised risk factors for AKI. Conclusion: Hospital based cross-sectional study design with selection bias, lead time bias and diagnosis bias which limits its potential to make conclusion. Estimated GFR (e GFR) using Schwartz formula is inferior to ideal measured GFR using cystatin-C or inulin and noble biomarkers for diagnosing AKI like KIM-1 & NGAL are quite expensive which was beyond the scope of our study.

Introduction: When sickled erythrocytes are present in the renal medulla, it causes ischemia, microinfarcts, and papillary necrosis in the kidneys. This condition is known as sickle cell nephropathy (SCN), which is the renal manifestation of sickle cell disease (SCD). Clinically presenting as increased GFR as a result of localised prostaglandin production and enhanced nitric oxide synthase in response to hypoxia, glomerular hyper filtration is the initial sign of SCN. This leads to an increase in renal blood flow and albuminuria 2. Proteinuria types 1 and 4 affect 20–30% of SCD patients. Material and Methods: We also measured height and weight using anthropometric techniques. The individuals’ shoes and top clothing were taken off before these measurements were taken. Every subject’s weight was recorded using digital weighing equipment, which was calibrated as needed and had its accuracy confirmed on a regular basis, to the nearest 0.1 kg. Using a portable stadiometer, the standing height was measured to the closest 1 cm. Weight (in kilogrammes) divided by height (in metres squared) was used to calculate BMI (kg/m2). Using a suitable blood pressure cuff size for the child’s upper arm and a relaxed forearm on the examination table, the resting Systolic blood pressure (SBP) was measured. Results: Similar to earlier studies, we discovered 5.83% of AKI patients in our investigation. According to Baddam S et al., 17% of vaso-occlusive pain crises had an AKI3 connection. Vasoocclusive pain crises were a frequent side effect in kids with SCA and a known risk factor for AKI, with 2.5–17% of kids admitted to the hospital due to a VOC going on to develop AKI136–38. Acute infection (malaria and sepsis), hypovolemia (insensible loss due to fever, reduced intake, diarrhoea, and vomiting), and the use of NSAIDs to manage Vaso-occlusive crises are recognised risk factors for AKI. Conclusion: Hospital based cross-sectional study design with selection bias, lead time bias and diagnosis bias which limits its potential to make conclusion. Estimated GFR (e GFR) using Schwartz formula is inferior to ideal measured GFR using cystatin-C or inulin and noble biomarkers for diagnosing AKI like KIM-1 & NGAL are quite expensive which was beyond the scope of our study.