20 cards Flashcards
which nephrotic syndrome is seen in autoimune diseases
Membranous glomerulonephritis
moa of calcium resonium
Calcium resonium results in removal of potassium from the body, rather than shifting potassium between fluid compartments in the short-term
Meds for hyperkalemia that stablises the cardiac membrane
IV calcium gluconate. Does not lower serum potassium levels
Meds for hyperkalemia that cause a short term shift in potassium from ECF to ICF
Combined insulin/ dextrose infusion and nebulised salbutamol
Meds in hyperkalemia that remove potassium from the body
Calcium resonium (PO or enema), loop diuretics, dialysis - hemofiltration/ hemodialysis considered for patients with AKI and persistent hyperkalemia
causes of acute interstitial nephritis
Causes
drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
iga nephropathy classic presentation
IgA nephropathy classically presents as visible haematuria following a recent URTI
mng of minimal change disease
prednisolone
what type of ABG result would you expect in DKA
raised anion gap metabolic acidosis
what type of ABG result would you expect in salicylate overdose
raised AG metabolic acidosis
What type of ABG would you expect in diarrhea
normal anion gap acidosis
Metabolic acidosis with a raised anion gap causes
usually associated with conditions where there is an accumulation of unmeasured acids, such as in diabetic ketoacidosis, lactic acidosis, or uraemia.
Metabolic acidosis with a reduced anion gap causes
educed anion gap is rare and often seen in hypoalbuminaemia (due to albumin being one of the unmeasured anions) or in the presence of abnormal proteins such as in multiple myeloma.
Metabolic alkalosis causes
the loss of acid (as in vomiting) or by bicarbonate retention (e.g., from diuretic use or in patients with hyperaldosteronism)
how to differentiste between causes of aldosteronism
Primary and secondary aldosteronism can be differentiated by looking at the renin levels. If renin is high then a secondary cause is more likely, i.e renal artery stenosis.
management of proteinuria in ckd
ACE inhibitors (or angiotensin II receptor blockers) are key in the management of proteinuria
they should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure
SGLT-2 inhibitors
patients who have proteinuric CKD (with or without diabetes) may benefit from treatment with SGLT2 inhibitors
they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria
by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure
normal AG
8-16 mmol/L.
type of anaemia in CKD
Normochromic normocytic
Why do patients with CKD get anaemia
Causes of anaemia in renal failure
reduced erythropoietin levels
the most significant factor in CKD causing anaemia
CKD is associated with a decrease in the production of erythropoietin, a hormone produced by the kidneys that stimulates erythropoiesis in the bone marrow
reduced erythropoietin levels → diminished red blood cell production
reduced absorption of iron
hepcidin is an acute-phase reactant
in CKD, hepcidin levels are often increased due to inflammation and reduced renal clearance
elevated hepcidin levels lead to decreased iron absorption from the gut and impaired release of stored iron from macrophages and hepatocytes, reducing the iron available for erythropoiesis
additionally, metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron (Fe³º) to its absorbable form, ferrous iron (Fe²º), in the duodenum → reduced iron absorption.
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss
management of anaemia in CKD
Iron studies should be conducted in people with stage 3-5 CKD as part of their regular assessment under the orange and red clinical action plans (see pages 27-28). This allows for earlier identification and treatment of anaemia. * In people with CKD, other forms of anaemia should be considered and excluded: − Iron deficiency (absolute and functional) is a common cause of anaemia in people with CKD. − If absolute iron deficiency is identified, causes including GI blood loss should be considered and excluded. − Vitamin B12 and folate levels should be checked and corrected if deficient. Note, long-term use of proton pump inhibitors (PPI) is associated with vitamin B12 deficiency. * Thyroid stimulating hormone should be assessed and hypothyroidism treated if present. * Both significant hyperparathyroidism and systemic inflammation may contribute to anaemia and may cause refractoriness to erythropoietin therapy. * Ensure adequately iron replete with either oral or IV iron. * Treatment with ESA must be managed by a nephrologist. There are several ESAs currently available for this indication in Australia. All are available as pre-filled syringes and are usually administered subcutaneously to those with CKD or on peritoneal dialysis patients and intravenously to those on haemodialysis.
