Flashcards in Renal Deck (44):
Name 5 causes of pre-renal acute renal failure
Pre-renal disease = hypoperfusion
1. Hypovolaemia - dehydration, third space sequestration (crush injury/skeletal fracture), blood loss
2. Effective volume depletion - CCF, liver cirrhosis, nephrotic syndrome
3. Severe hypotension - sepsis (systemic vasodilatation), myocardial infarct
4. selective renal ischaemia - renal artery stenosis, hepatorenal syndrome
5. Drugs - NSAIDs, ACEi
How do NSAIDs cause acute renal failure?
inhibit prostaglandin synthesis leading to increased preglomerular resistance (renal PGs = vasodilator)
How do ACE inhibitors cause acute renal failure?
In disorders where intrarenal perfusion perssure is reduced, GFR is maintained in part by Ang II-mediated increase in resistance at the efferent arteriole.
Blocking this response with an ACEi will cause relaxation of the efferent arteriole, lower intraglomerular pressure and reduced GFR
What is acute tubular necrosis?
A renal cause of acute renal failure.
Abrupt and sustained decline in GFR within minutes-days after ischaemic/nephrotoxic insult. GFR declines to prevent life-threatening loss of electrolytes from non-functioning tubules
Name 4 classes of drugs that can cause ATN.
1. Antibiotics - aminoglycosides, amphotericin B, cephalosporins
2.Antiviral - cidofovir
3. Chemo - cisplatin, methotrexate
What are the most common causes of benign haematuria?
Menstruation, vigorous exercise, trauma, sexual activity
What are the most common causes of extrarenal haematuria?
Malignancy (kidney, badder, prostate)
Infection (esp. cystitis, prostatitis)
What are the most common causes of intrarenal haematuria?
Sickle cell trait or disease
Generally what colour does blood coming from the glomerulus give urine?
Dark, cola appearance
What do dysmorphic RBCs in the urine signify?
Glomerular source of haematuria
What do RBC casts in the urine signify?
What is nephrotic syndrome characterised by? (4)
Protein excretion of more than 3g per 24h
What is the typical clinical presentation of minimal change disease?
Oedema, ascites in a child younger than 10 years; and onset over days to weeks. Can affect older individuals.
How common is minimal change disease?
Accounts for approx. 90% of nephrotic syndrome in children aged less than 10 years; accounts for approximately 20% of nephrotic syndrome in adults
What are the characteristic lab findings of minimal change disease?
Nephrotic syndrome, normal renal function and normal urinary sediment except for hyaline casts and oval fat bodies. Rarely, renal insufficiency may be present.
What is the appropriate management of minimal change disease?
Prednisone 4-8 weeks; gradually taper if a response is noted. ACE inhibitors may also be used as an adjunct to therapy (to further reduce proteinuria) or as sole therapy in mild cases
What are the complications of minimal change disease?
Peritonitis in children; cushingoid effects of steroid therapy; and rarely AKI (reversible)
What is the most common cause of nephrotic syndrome in adults?
Focal segmental glomerulosclerosis
What is the typical clinical presentation of membranous nephropathy?
Oedema, usually with gradual onset over weeks to months; BP may be normal or elevated
What is the typical clinical presentation of IgA nephropathy?
Gross haematuria during viral URTI or GI illness, persistent microscopic haematuria and sometimes associated dull flank pain
What are the most common conditions with which IgA nephropathy is associated? (4)
2. Chronic liver disease (e.g. alcoholic cirrhosis)
4. Coeliac sprue
What are the renal findings associated with diabetic nephropathy?
Microalbuminuria, then frank proteinuria often progressing to nephrotic syndrome associated with gradual decrease in renal function over a period of 5-10 years
What are the renal biopsy characteristics of diabetic nehropathy?
Deposition of periodic acid Shiff (PAS)-positive material in the glomerula mesangium sometimes in nodular form (KW lesions) and in the afferent and efferent arterioles of the glomeruli
What is the pathogenesis of Goodpasture syndrome?
Antibody formation to the alpha3 chain of type IV collagen in the GBM
When do patients with Goodpasture present and who is affected?
Most common in meg, ages 20-40 and 50-70 years; occurs more commonly in smoker of those with lung injury
What is the typical clinical presentation of Goodpasture syndrome?
Malaise, rapidly progressive renal failure, anaemia and pulmonary haemorrhage
What are the renal biopsy characteristics of Goodpasture syndrome?
Crescentic GN with linear deposition of IgG along the GBM on immunofluorescence
How can intrinsic renal disease be divided into?
1. Vascular - vasculitis (Wegener's granulomatosis, microscopic PAN), scleroderma, malignant hypertension
2. Glomerular - nephritic vs nephrotic
3. Interstitial - ATN, drug toxicity, AIN, tumour lysis
What is the common cause of tubular/interstitial renal disease?
Acute tubular necrosis
What are the classic features of drug-induced AIN?
Classic features = triad of fever/rash/eosinophilia, triad rarely present.
Usually non-specific symptoms (N&V, malaise, lethargy) or no symptoms at all
List 4 drugs that can cause acute interstitial nephritis
Antibiotics - penicillins, sulfonamides, ciprofloxacin, rifampicin
List 5 causes of acute interstitial nephritis
1. Drugs (70%)
How is Stage I CKD defined?
eGFR > 90mL/min
How is Stage II CKD defined?
eGFR 60-90 mL/min
How is Stage III CKD defined?
eGFR 30-59 mL/min
How is Stage IV CKD defined?
eGFR 15-29 mL/min
How is Stage V CKD defined?
eGFR less than 15 mL/min
At what GFR does end stage renal disease generally occurs?
At what point is renal failure considered to be chronic?
Most episodes of AKI resolves within 2-3 months. Therefore a patient is considered to have CKD when decreased GFR has persisted for more than 3-6 months
What are te renal US findings in patients with CKD?
Small, echogenic kidneys
How does bone disease in CKD come about?
1. As GFR falls, P04 excretion falls but intake does not
2. Serum PO4 thus begins to rise.
3. Considering Ca and PO4 are reciprocals, increase in PO4 results in decrease in serum Ca (Ca + PO4 leads to CaPO4)
4. The fall in serum calcium stimulates PTH production
5.PTH attempts to restore serum calcium by mobilising Ca from bone and upregulating the excretion of remaining functioning nephrons
RENAL BONE DISEASE
What is the most common cause of CKD in Australia?
What is Brenner's theory of hyperperfusion and hyperfiltration?
As primary renal disease progresses, the pool of surviving function nephrons declines causing afferent arterioles to dilate and efferent arterioles to contract --> increase intra-glomerular capillary flow --> overall GFR maintained
BUT can induce glomerular HTN --> perfusion injury --> glomerulosclerosis --> loss of glomerlui and decrease in GFR