to explain the rise in Cr and ≥10% rise in serum cystatin levels from baseline at 24 h. Cr will be assessed at baseline and at 24, 48 and 72 h and CyC will be measured at baseline and at 24 h. Results: After 48 hrs of CM exposure, Cr increase ≥0.5 mg/dL occurred in 29 patients (11.3%) whereas increase in CyC ≥10% at 24 hrs after CM exposure occurred in 66 patients (26.08%). The difference in mean Cr and baseline, 24 hrs and 48 hrs after CM exposure was not statistically significant whereas that between CyC at baseline and 24 h after CM exposure was significant. CyC detected CIN 24 hrs earlier as compared to Cr. Similarly the difference between GFR calculated by Cr equation was not statistically significant between pre and post CM exposure but the difference was significant when GFR was calculated using the combined equation. The risk of CIN was higher in patients with pre-existing CKD, diabetes, advanced age, haemodynamic instability, heart failure (LVEF < 40%), patients with ACS and higher contrast volumes. Conclusions: The assessment of CyC at 24 hours after CM exposure allows an early diagnosis of CIN. Also CyC equation and the combined equation (Cr + CyC) for measurement of GFR accurately identified the patients with CIN even at 24 hrs after CM exposure, in contrast to Creatinine which took 48-72 hrs. Hence the management strategies for CIN can be started earlier by 24-48 hrs when CyC is used as a marker for CIN which would improve long term outcomes.

Patients with Nephrotic syndrome have increased tendency for thromboembolism. Pulmonary thrombo-embolism is life threatening complication. We report a case of 3 yrs old patient a known case of Nephrotic syndrome with bronchial asthma who presented with severe respiratory distress requiring ventilatory support. He was diagnosed with massive bilateral pulmonary embolism and treated successfully with thrombolysis.

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