Internal assessment: 

Antomocal Diagnosis: glomerulus of kidney

Histological: ? Loss of effacement of foot process of podocytes of basement membrane

? Membranous glomerulopathy

Etiological: diabetes and hypertension.

Diabetic nephropathy

  

2.azotemia :

Increased blood urea nitrogen with BUN to creat ratio 20:1 suggestive of renal or post renal azotemia.

https://www.ncbi.nlm.nih.gov/books/NBK538145/

 https://www.ncbi.nlm.nih.gov/books/NBK538145

Anemia:https://pubmed.ncbi.nlm.nih.gov/6876938/

https://spectrum.diabetesjournals.org/content/21/1/12

Hypoalbuminemia:

Reduced protein intake and inflammation,due to reduced production of albumin by liver leading to decreased synthesis and increased catabolism and vascular permeability.

https://pubmed.ncbi.nlm.nih.gov/9848794/

Acidosis: renal failure as there is decreased synthesis of bicarb resulting in high aniono gap metabolic acidosis.

https://pubmed.ncbi.nlm.nih.gov/6876938/

3.according to KDIGO guidelines,oral replacement therapy is initiated when plasma hco3 is less than 22 meq/lit

IV replacement formula : hco3 =0.5×wt (kg)×  (24-serum hco3) or desired increase in hco3.


https://www.uptodate.com/contents/sodium-bicarbonate-drug-information?topicRef=127552&source=see_link#F221615

Bicarb deficit for this patient weight being 55 kgs is 300meq/lit, therefore a bolus dose of 150meq/lit was given followed by oral replacement till decision for hemolysis was made.

In patients of ckd bones release bicarb and phosphate by process of demineralisation to compensate for the additional acid being accumulated,thus causing osteopenia, there fore oral bicarbonate therapy to counter this effect .

4.on the day of admission egfr 7.5ml/min/1.73m2 with urine output less than 100ml in 24hrs with high anion gap metabolic acidosis.

Patient showed metabolic acidosis on day 3,hence taken up for hemodialysis.

5 . Infection causing AKI 

? Iga glomerulonephritis

Lupus nephritis

Renal aretery stenosis.

https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd/causes

7.mechanism of hfpefr in renal disease


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

10.https://jasn.asnjournals.org/content/21/2/223

2nd question:

Diagnosis: pre renal AKI ( BUN more than 20:1) on CKDs to diarrhoea and dehydration. 

Conservatively managed with adequate fluids.

Anemia and hypoalbuminemia would point out CKD,but patient is having adequate urine output and fluids,hence dialysis is not initiated 

Usg findings in 1st patient: kidney size normal and increased echogenicity ,but normal size can be due to diabetic nephropathy

2nd patient : normal size and echotexture.













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