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)
Goodpastures syndrome
haemoctasis and glomerulonephritis
Can be due to vasculitis or streptococcal infections
Good pastures disease
- what
- therapy
attack of the basement membrane
- prednisone, cyclophosphamide, plasma exchange, HD
What are the two most common environmental factors for hypertension?
obesity and high salt intake
First line treatment for hypertension
Lifestyle modification
- weight loss
- Low sodium diet
- exercise
Younger patients vs older patients, what is the hypertension generally caused by?
younger: RAAs (so use ACEi’s)
55yrs
Older: sympathetic nervous system (diuretics/ CCBs)
Indications.. for each disease treat with?
- IHD
- CHF
- DM
- CKD
- Beta blocker
- Thiazide/ACEi/ ARB/ B-blocker
- ACEi/ARB/ thiazide
- ACEi/ ARB
Resistant hypertension defined by
BP not at target despite optimal dose of three complimentary drugs of which one is a diuretic
Causes of resistant hypertension
Not giving drug in proper dose non-compliance competing drug (sodium, NSAIDs, OCP)
Secondary(non-essentil causes of hypertension)
Endocrine - phaeo, Conn’s, hyperthyroid
Renal - GN, CKD, RAS
OSA (obstructive sleep apnea) high liquorice intake
Drugs you should never combine
ACEi and Beta-Blocker
ARB and B-blocker
ACEi and ARB
How do you detect masked hypertension
24hour ambulatory BP
What is white coat hypertension
When BP high in the clinical but low out in the public (measured via ambulatory monitoring)
UTIs - where?
Cystitis - infection of the bladder
Pyelonephritis - infection of upper urinary tract
treatment are antibiotics
In women versus men
women: quite common, almost one a year in sexually active women
In men always considered complicated
Uncommon
treat with antibiotics
consider prostatitis and urethritis
UTIs in pregnant women
2-7% of pregnancies
smooth muscle relaxation and ureteral dilation
Increased risk of preterm birth, low with weight and perinatal mortality
Treatment reduces complications
pylonepritis in pregnant women treat with?
IV antibiotics
What if recurrent infections
> 2 infections in 6 months are > 3 infections in a year
If not associated with abnormal urinary tract then should not cause disease
Recurrent cystitis not infrequent
Recurrent pylonepritis uncommon
pathogenesis
most uropathogens originate in the rectal flops, colonise the pariurethral / urethral area and ascend to the bladder
Increasing evidence that alteration of the normal vaginal flora may predispose women to introital colonisation and UTI
Relapsing UTI
the same strain coming back within two weeks of original infection
Reinfection UTI
UTI arising more than two weeks after treatment even if pathogen is the same as the original
When a sterile urine culture is documented between the two UTIs in a patient off antibiotics
UTI risk factors
Genetics - increased sussceptibitliy to uropathogens Behaviours Anatomy Post menopausal women - incontenince - cystocele - Postvoid residual
prevention
altered behaviour - contraception - postcoital void/ fluid - cranberry juice Antimicrobial prophylaxis - continuous - post coital - intermittent self treatment Topical oestrogen in postmenopausal women
ESRD treatment options
Conservative Dialysis - peritoneal - haemodalysis Renal transplant - deceased donor - Live donor
Why is the are we getting more ESRD in the population
A lot of ESRD is in the elderly
So in young people the rates are pretty similar but people are living longer, serving longer with their cardiovascular disease and having complications of ESRF
In what cases would you manage a patient with ESRD supportively rater than offer transplant etc.
look at illness trajectory
Does the patient have other morbidities that would prevent them from having renal replacement therapy E.g. terminal cancer, stroke, heart failure, dementia
