L24 Clin prob solve 2: Kidney failure

Question 1

Define kidney failure

Answer 1

Reduction in GFR

Question 2

What are different features of AKI compared to CKI

Answer 2

AKI is usually reversible and secondary to another illness- deterioration over short amount of time.

CKI generally has fluid overload, malnutrition, rash from high phosphate, Pth, pericardial rub from toxins sounds like crunchy snow. Kidney less than 8cm highly likely to be due to CKI but is not exclusive. Mainly caused by diabetes, hypertension, glomerular disease.

Question 3

What are signs associated with the 3 causes of Acute renal failure- how to differentiate between them

Answer 3

Pre-renal: Due to decreased perfusion of kidneys so has low BP - sepsis, HF, dehydration, bleeding etc which can progress to intrinsic renal->

Renal: Mainly Acute Tubular necrosis due to untreated pre-renal: aminoglycosides, contrast, NSAIDS, Rhabdomyolysis. Other causes is Rapidly progressive glomerularnephritis- crescents in glomeruli on biopsy, RBC and casts in urine- haematuria. Which can lead to Nephritic syndrome

Post renal: Obstruction along the ureters onward - seen best on renal ultrasound- dilation of the renal pelvis. Due to tumours, stones, fibrosis

Question 4

What are the blood tests that help to differentiate Acute or chronic

Answer 4

For both, K+, urea, creatinine and Phosphate are increased because the kidney is not getting rid of it properly.
Hb is low in CKI because kidney damage reduces EPO therefore the number of RBCs- and Hb. However RBCs have life of 120 days so they have to die first for this effect to be prominent
Also expected to see high parathyroid hormone in CKI

Question 5

What are the consequences of high serum phosphate due to kidney failure

Answer 5

1. Causes increased secretion of fibroblast growth factor23 in the bones which reduces phosphate absorption in the gut
2. reduces active vitamin D
3. –> reduces Ca2+ absorption which increases parathyroid hormone ( secreted when low Ca/high phosphate).
4. Causes excessive bone reabsorption of Ca2+, taking it out of the bones, increases vit D production and increased renal excretion of phosphate
5. However this causes increased risk of fracture, or extraosseous ossification in the blood vessels which stops distension and makes inner surface rough- promotes clotting by platelets
6. Can lead to obstructive ischaemia- stroke, vascular disease

Question 6

How is CKD managed

Answer 6

1. BP reduced using ACE inhibitors: stopping vasoconstriction by Ang2 so vasodilates, reduces Na+ and water reabsorption and dilates the efferent arteriole to reduce Glomerular BP and help to prevent further damage
2. If GFR still reasonable -eg 30, glycaemic control can also be helpful for diabetics,
3. Treat the anaemia
4. Dialysis to keep them alive while waiting for their kidneys to get better