General Renal Flashcards
What is Calciphylaxis?
Presents as painful rash, typically ulcerated lesions to the lower limbs
Skin ischaemia/necrosis due to calcification of capillaries/arterioles
Why are acidosis and K+ linked from a kidney perspective?
H+ is exchanged for K+ in the kidneys
When there are high H+ levels these will be excreted by the kidneys but in exchange K+ will be brought back into the bloods
When H+ is low K+ is exchanged into the urine and lost to hold onto H+
Acidosis > hyperkalaemia
Alkalosis > hypokalaemia
Why does bicarb (HCO3) drop in metabolic acidosis?
HC03 acts as a buffer and combines with H+ ions to form H20 and Co2
If hydrogen ions are high but C02 is low then bicarb will preferentially combine with H+, leading to depletion of bicarb
If CO2 is high (resp acidosis) then this pushes the equilibrium in the other direction creating more bicarb and H+
Why is bicarb administration for metabolic acidosis controversial?
Increasing the plasma bicarbonate level will reduce the hyperventilatory respiratory drive, leading to a less marked hypocanoea.
The partial pressure of CO2 is reflected more quickly across the blood brain barrier, which can lead to temporary worsening of cerebral acidosis and thus the potential for worse neurological outcomes
However the evidence is not clear either way
What is the Urea:Cr ratio?
Used to determine the rough cause of an AKI
Pre-renal = >100:1
Post Renal/Normal = 40-100:1
Renal (ie ATN) = <40:1
Urea measured in mmol/L, but Cr in umol/L, thus divide the Cr by 1000 to get mmol/L
Ie Urea 39mmol/L and Cr 351umol/L
39/0.351 = 111, thus cause is pre-renal
What are other causes of a raised Ur:Cr ratio other than pre-renal AKI?
Either over production of urea or under production of creatinine
- GI haemorrhage (most common)
- Corticosteroids
- High protein diet
- Severe catabolic state
What are the indications for renal tract imaging in pyelonephritis?
Shock
Significant renal impairment
Significant PHx of renal calculi
Single kidney
Immunosuppressed
Failure of outpatient management
What are the differentials for new onset large volume polyuria? What is the definition?
> 3L/Day in adults
2L/m2 in kids
Solute Diuresis
- T1/2 diabetes
- mannitol
- Post IV fluid administration
- Elevated urea from tissue catabolism (ie glucocorticoid use)
- SGLT-2 use
Water diuresis
- Neurogenic diabetes insipidius
- Nephrogenic diabetes insipidus (ie lithium related ADH insensitivity)
- Psychogenic polydipsia
- Phenothiazine related polydipsia
- Diuretic abuse
- Post obstructive diuresis
What tests would you perform in new onset polyuria?
BSL
- assess for DM
Serum osmolality
- Decreased in polydipsia
Serum sodium
- Decreased in polydipsia but elevated in diabetes insipidus
Urine Osmolality
- <300mosm/kg = water diuresis, >600 = solute diuresis, inbetween is grey
What are the diagnostic criteria for SIADH?
- Clinically euvolaemic
- Serum osmolality <275
- Urine osmolality >100
- Urine Na+ >20
- Hyponatraemia without another obvious cause