Renal Problems - de Zoysa Flashcards
Approach to AKI
Identify patient at high risk and optimise care Stop all neurotoxic agents assess and optimise volume status Monitor creatinine and urine output non-invasive diagnostic workup Invasive diagnostic workup Revise drugs Diet
What role could NSAIDs play?
NSAIDs block prostaglandins PGE2 vasodilatory NSAIDs cause increase in PGE2 causing vasoconstriction Decreased renal blood flow Decreased GFR
Get increased renin secretion because NSAIDs reduce renin
Can cause:
- AKI
- Minimal change
- Acute interstitial nephritis
ways to asses patients volume status at bedside
JVP capillary refill time Pulse, check volume, rate and rhythm (tachycardia suggests low BV) Blood pressure Tissue turgor... Peripheral oedema
Blood in the urine highly suggestive of?
glomerulonephritis
if patent has pyurea and proteinuria its suggestive of?
Inflammation, most commonly caused by infection but can also be caused by tubular interstitial nephritis, which can also be caused by anti-inflammatory drugs
What can you do as a next step in investigation if renal ultrasound doesnt work?
biopsy kidney
CKD is based on?
Cause, GFR category and albuminuria category
What is the common pattern observed in abnormalities of calcium phosphate observed in CKD?
progressive hypophosphataemia
in the later stages hypoclaememia
What is the most common type of haematological problem seen in CKD
Anaemia nomochromic, normochromic expected
Glomerulonephritis can be caused by?
- Nephrotic syndrome
- Nephritic syndrome
- Rapidly progressive GN
- Asymptomatic urine abnormalities
- AKI
- CKD
What is neurotic syndrome characterised by?
heavy proteinuria
causing albumin levels to drop in plasma,
causing fluid to leak from the vascular space into the interstitial space –> peripheral edema
(triad of symptoms)
Nephritic syndrome characterised by?
Haematuria (macro or microcytic)
proteinuria, with this we will collect salt and water, get peripheral edema, hypertension and deteriorating renal function
= blood and protein in urine, oedema and hypertension
Rapidly progressive GN characterised by?
progressive renal deterioration, and crescents on renal biopsy
Crescents on renal biopsy
extra cells that are proliferating in bowmans space
–> a non-specific response to injury of the capillary wall
physical gaps appear in the filtration barrier
“rents” allow circulating cells, inflammatory mediators, and plasma proteins to enter into bowmans space
The contents in bowmans space can enter the intersitium, contributing to periglomerular inflammation
The severity of GN is associated with
the degree of crescent formation
In early stages this is reversible
crescents are a non-specific response
Classification of Rapidly progressive glomerular nephritis
Anti- GBM disease
Immune complex
- e.g. post infectious, lupus nephritis
Pauli-immune (when all stains are negative)
