5th September exam

Patient 1-
1- Based on history and investigations -

There is acute Rapidly progressive Glomerular damage ( superimposed on  Diabetic Nephropathy ) -The rate of decline in GFR is more than expected in Diabetic nephropathy-
There could be and added glomerular injury complicating Daibetic nephropathy

https://jamanetwork.com/journals/jama/fullarticle/369422.Here they present 2 such cases who presented with rapidly progressive renal failure .I quote few lines from the journal - 

However, in both patients the rate of loss of glomerular
filtration rate was greater than that usually seen in diabetic glomerulosclerosis, and the urine sediment contained many RBC casts. These findings led to
renal biopsy, which demonstrated crescentic glomerulonephritis superimposed on diabetic glomerulopathy. Both patients were treated with predni-
sone and cyclophosphamide and both experienced substantial improvement
in renal function.)))

Other possibilities - Lupus nephritis ,IgA nephropathy

Anemia- Microcytic hypochromic - ? probably due to Iron deficiency Anemia

In the background of Diabetes and hypertension with 4+ albuminuria ,and hypoalbuminemia there is probablilty of Glomerular damage. 

2-  Rapid decline in GFR causing retention of nitrogenous waste products - leading to increased serum creatinine and urea .
In this case as the urine analysis is suggestive of glomerular damage - there is decline in GFR with reduced urine output . Most likely it could be Renal azotemia .

Retic count suggestive of hypoproliferative anemia
Peripheral smear-suggestive of Microcytic hypochromic anemia
Could be Iron deficiency anemia - /chronic inflammation 
Chronic inflammation leads to increase in serum ferritin ,also increase in hepcidin levels that inhibits  absorption of serum iron from GIT and inhibits release of stored iron . along  with this there is  decrease in erythropoietin synthesis .

- As Spot urine Protein and 24hrs urine protien suggestive of significant protienuria .
  Hypoalbuminemia could be due to glomerular damage causing albuminuria .

- Acidosis - Glomerular disease will cause decreased Glomerular filtration rate --Hence there is defect in Tubular secretion of acid and reabsorption of bicarbonate .leading to retention of Acid and bicarbonaturia- producing metabolic acidosis .

- 3- Bicarbonate supplements slows progression of CKD and improves nutritional status - Open label ,randomised prospective study! Baseline patient characteristics were matched equally in both groups . It was conducted in patients with mild metabolic acidosis Hc03 more than 16 but less than 20 ,with stable condition .

https://jasn.asnjournals.org/content/20/9/2075

 P-Total 134 ppl enrolled and they are randomised

Finalanalysis-67 in bicarbonate group and control group

I- sodium bicarbonate-oral tablets dosage 1.82+-0.80g/d
C-standard treatment vs sodium bicarbonate
O- Rate of decline in crcl was similar in two groups at 12 months because of dropout of 17 pt from control group .Rate of decline in sodium bicarbonate group was significantly lower than control after 12 month .
( 1.88 crcl in bicarbonate group ,5.9 in control group )
9 outof 63 pt in bicarbonate group and 20/43 pt in control group  underwent rapid progression to CKD

4 pt in bicarbonate and 22 pt in control required dialysis
Nutritional improvement - Midarm circumference increased in bicarbonate group from 24.8 to 26.3 compared with no change
Increase in calorie intake in bicarbonate group vs control group 

4- As patient was anuric ,with severe pedal edema , facial puffiness , subcutaneous edema with severe metabolic acidosis .
Patient was taken for hemodialysis
Chronic metabolic Acidosis in CKD  could worsen further renal damage along with other effects like bone disease , protien catabolism ,CV disease ,decreased albumin synthesis .

 https://jasn.asnjournals.org/content/31/3/469

Metabolic acidosis in CKD stimulates production of intrakidney paracrine hormones including angiotensin II, aldosterone, and endothelin-1 (ET-1) that mediate the immediate benefit of increased kidney acid excretion, but their chronic upregulation promotes inflammation and fibrosis. Chronic metabolic acidosis also stimulates ammoniagenesis that increases acid excretion but also leads to ammonia-induced complement activation and deposition of C3 and C5b-9 that can cause tubule-interstitial damage, further worsening disease progression.

In animal models, prolonged acid exposure directly damages kidney substructures, such as podocytes and the glomerular filtration apparatus, and disrupts the signaling within proximal and distal tubules that is needed to maintain acid-base balance
Anuria with severe metabolic Acidosis was the main indication for dailysis

5- Either idiopathic or systemic inflammation ,Or infection super added on native Daibetic and Hypertensive kidney Disease would be the reason of rapidly progressive renal failure .

6-https://jasn.asnjournals.org/content/7/5/728

adverse impact of hypoalbuminemia may have
been partly mediated by cardiac dysfunction. Hypoalbuminemia was independently associated with
echocardiographic abnormalities, de nova cardiac failure, recurrent cardiac failure, de nova ischemic heart
disease, and recurrent ischemic heart disease. The analyses shown strongly suggest that low serum albumin levels came before these adverse events, and
not vice versa. Preliminary reports from other investigators suggest an independent association between
hypoalbuminemia and cardiac mortality

7- given the patient history although she developed SOB acute onset , patient denied palpitations,orthopnea,PND that would suggest acute left ventricular failure . If the patient had such symptoms cardiorenal syndrome would be one of the possibility .

Patient 2:
Patient had similar complaints when he presented ,but after placing Foley's patient passed substainal amount of urine .And he was lasix resposnosive and urine output was maintaining .His acidosis ,and azotemia resolved during hospital stay. Hence both clinical and biochemical parameters helped in delaying dailysis for the patient .