Renal Flashcards
what is the normal ACR for an adult?
increased urinary albumin:creatinine ratio (>3.5 mg/mmol for women or >2.5 mg/mmol for men)
what is the treatment for diabetic nephropathy?
- dietary protein restriction
- tight glycaemic control
- BP control: aim for < 130/80 mmHg
- ACE inhibitor or angiotensin-II receptor antagonist -
should be start if urinary ACR of 3 mg/mmol or more - control dyslipidaemia e.g. Statins
what is the treatment for lupus nephritis?
Lupus nephritis is initially managed with high-dose steroids alongside either mycophenolate or cyclophosphamide. The preferred treatment for maintenance is mycophenolate.
what are the WHO classification of lupus nephritis?
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
what is the most common form of lupus nephritis and how it is treated?
Class IV (diffuse proliferative glomerulonephritis) is the most common and severe form. Renal biopsy characteristically shows the following findings:
glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
if severe, the capillary wall may be thickened secondary to immune complex deposition
electron microscopy shows subendothelial immune complex deposits
granular appearance on immunofluorescencew
whats the difference between contrast media toxicity and nephropathy?
Contrast media nephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media.
Contrast-induced nephropathy occurs 2 -5 days after administration.
what is the treatment for contrast nephropathy?
the evidence base currently supports the use of intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate
what are features of rhabdomyolysis?
- acute kidney injury with disproportionately raised creatinine
- elevated creatine kinase (CK)
- the CK is significantly elevated, at least 5 times the upper limit of normal
- elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology
- myoglobinuria: dark or reddish-brown colour
- hypocalcaemia (myoglobin binds calcium)
- elevated phosphate (released from myocytes)
- hyperkalaemia (may develop before renal failure)
- metabolic acidosis
what is IgA nephropathy linked to?
There is a higher incidence of IgA nephropathy in patients with coeliac disease and dermatitis herpetiformis
Henoch scheloin purpura
alcoholic cirrhosis
what is the difference between post strep GN and IgA nephropathy?
- post-streptococcal glomerulonephritis is associated with low complement levels
- main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
- there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis
what is the treatment for IgA nephropathy?
Isolated hematuria, no or minimal proteinuria (less than 500 to 1000 mg/day), and a normal glomerular filtration rate (GFR) - no treatment needed, other than follow-up to check renal function
persistent proteinuria (above 500 to 1000 mg/day), a normal or only slightly reduced GFR - initial treatment is with ACE inhibitors
if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors - immunosuppression with corticosteroids
what percentage of IgA nephropathy go into ESRF?
25%
what is a good prognostic marker of IgA nephropathy?
frank haematuria
what is a bad prognostic marker of IgA nephropathy?
male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD
what are the causes of HAGMA?
M — Methanol
U — Uremia (chronic kidney failure)
D — Diabetic ketoacidosis
P — Paracetamol, Propylene glycol (used as an inactive stabilizer in many medications; historically, the “P” also stood for Paraldehyde, though this substance is not commonly used today)
I — Infection, Iron, Isoniazid (which can cause lactic acidosis in overdose), Inborn errors of metabolism (an especially important consideration in pediatric patients)[7]
L — Lactic acidosis
E — Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)
S — Salicylates
what are the causes of NAGMA?
- gastrointestinal bicarbonate loss:
prolonged diarrhoea: may also result in hypokalaemia, ureterosigmoidostomy, fistula - renal tubular acidosis
- drugs: e.g. acetazolamide, ammonium chloride injection
- Addison’s disease
when do you treat secondary hyperparathyroidism in CKD?
When PTH is twice as normal
