Internal assessment

 1 .AKI secondary to ?Nephrotic syndrome secondary to uncontrolled diabetes mellitus, hypertension with Anemia https://www.ncbi.nlm.nih.gov/books/NBK538145/ 

2. Azotemia due to worsening of third spacing from intravascular depletion (pedal edema , ascites) and poorly controlled diabetes and hypertension 

Anemia due to decreased levels of erythropoeitin which is produced in kidney

 Hypoalbuminemia due to damage to glomerulus which increases albumin loss in urine. Chronic diseases like hypertension and diabetes also lead to albuminuria

 Acidosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5648741/ 

Acidosis due to decreased tubular reabsorption of bicarbonate and its decreased production in relation to amount of acid synthesized 

 3. Sodium bicarbonate to correct acidosis 

Kcl to correct hypokalemia .

Actrapid insulin for management of diabetes https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6341062/ https://pubmed.ncbi.nlm.nih.gov/14760875/ 

Lasix to increase urine output and reduced fluid overload Telmisartan to decrease proteinuria and hypertension Orofer xt and epo to correct anemia 

https://www.ncbi.nlm.nih.gov/books/NBK159869/ https://pubmed.ncbi.nlm.nih.gov/18322160/ https://www.hindawi.com/journals/tswj/2014/627673/ 

4. Dialysis was done as there is no improvement in urine output and acidosis inspite of treating it conservatively for 2 days 

 5. It can be due to nephrotic syndrome 

 6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759988/ 

the indications to apply RRT (1) severe azotemia with BUN >100 mg/dL, (2) metabolic acidosis, when arterial pH was <7.2 despite administration of intravenous bicarbonate, (3) dyselectrolytemia commonly serum potassium of more than 6 mEq/L despite antikalemic therapy, and (4) fluid overload causing pulmonary edema not responding to large doses of intravenous furosemide (60–120 mg). During period-2, some modifications were done for initiation of RRT based on the emergence of new knowledge that severe organ edema caused increased mortality and acidosis was an independent risk factor for death in our population during the study period-1 (unpublished results). During study period-2, RRT was initiated when pH was <7.25 and when severe fluid retention was present despite diuretic trial. Prolonged anuria was less frequently endured during period-2.

 7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6737277/ 

cardio-renal syndrome describes the co-existence of HF and chronic kidney disease (CKD). Approximately 50% of the patients with HFpEF also suffer from CKD .

 Although this co-existence is partially due to shared risk factors, such as hypertension, DM and obesity, it has also been proposed that HF directly impacts kidney function, and vice versa, CKD worsens cardiac function. Interdependence of the heart and kidneys, similarities between their microvascular networks, and the coexistence of CKD and HF further imply a role for microvascular dysfunction in development and progression of both diseases. https://images.app.goo.gl/rhx8AfbS4BRvahEA9 

8.In patients with CKD-associated anemia, iron supplementation is intended to assure adequate iron stores for erythropoiesis, correct iron deficiency, and, in patients receiving ESA treatment, prevent iron deficiency from developing. Iron supplementation, particularly with intravenous iron, can enhance erythropoiesis and raise Hb levels in CKD patients with anemia even when TSAT and ferritin levels are not indicative of absolute iron deficiency, and even when bone marrow studies reveal adequate iron stores.Iron treatment, particularly when administered intravenously, has also been consistently demonstrated to improve the erythropoietic response to ESA treatment. For any individual patient the optimal balance of Hb level, ESA dose, and iron dose at which clinical benefit is maximized and potential risk is minimized 

9. https://pubmed.ncbi.nlm.nih.gov/31729710/ Decreased protein intake leads to decreased synthesis of visceral proteins which causes hypoalbuminemia and leads to extravascular fluid accumulation

 2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991538/