CKD and Glomerulonephritis Flashcards
What is chronic kidney disease?
Progressive stepwise deterioration of renal function over months to years, that is often irreversible.
What values for eGFR dictate each stage of CKD?
Stage 1 -90+. (Evidence of anatomical defect or CKD) Stage 2 - 60-89. Stage 3a - 45-59. Stage 3b - 30-44. Stage 4 - 15-29. Stage 5 - <15.
What is used to determine if a patient has proteinuria?
Albumin creatinine ratio. Value of 30-290mg/g indicates microalbuninurua, whereas >300mg indicates overt proteinuria
What are primary causes of CKD?
Polycystic kidney disease,
Acute tubular necrosis,
Recurrent pyelonephritis,
Glomerulonephritis.
What are secondary causes of CKD?
Diabetes mellitus (lead cause),
Hypertension,
Renovascular disease,
Autoimmune (eg lupus).
What is the gross pathology of CKD?
atrophy and loss of renal parenchyma (kidney appears shrunken and cortex is replaced by extracellular matrix)
Why is HbA1c not used to measure diabetic control of a patient with CKD?
it is haemaglobin dependant and CKD commonly causes anaemia due to chronic disease, iron deficiency or lack of EPO secretion.
What type of diuretics should be used to treat oedema secondary to fluid overload caused by CKD?
What dosage should be used?
Loop diuretics (eg furosemide). Greater dosage required
Why may metabolic acidosis occur in patients with CKD?
Renal loss of bicarbonate. Treated with oral sodium bicarbonate tablets.
Why might a patient with CKD develop secondary hyperparathyroidism?
Kidney no longer activates vitamin D, so hypocalcaemia occurs. PTH rises to supply the body with calcium from bone in abscence of the negative feedback provided by calcium.
What skeletal problems are common in CKD?
Osteomalacia or rickets - due to bone resorption and high PTH levels.
What may occur after bone resorption in CKD and a rise in circulating free calcium?
Calcium deposition in tissues eg blood vessels or joints, leading to necrotic lesions - calciphylaxis
What may be required in a patient with CKD to manage calcium levels?
Parathyroidectomy
At what point do patients often require dialysis to survive?
End stage renal failure - when eGFR is around 8-10
What three treatment options does a person with end stage renal failure have?
Haemodialysis,
Peritoneal dialysis,
Renal transplant.
What are the benefits of haemodialysis?
Less responsibility placed upon the patient - good if young or elderly.
Proven to be effective long term.
Does not have to be undertaken every day - gives some freedom.
What are the drawbacks of haemodialysis?
Time consuming,
Rigid dialysis timing,
Access problems with fistulae,
Fluid and sodium restrictions to diet are often difficult to follow.
What are the benefits of peritoneal dialysis?
More independace - patients can change their own bags.
Less fluid and food restrictions.
More flexible schedule,
May preserve renal function better initially.
What are the drawbacks of peritoneal dialysis?
Infection (peritonitis).
Frequent overnight changes required.
Responsibility is placed on patient.
Less long term survival data.
What are the downsides of renal transplant? (This is still always the best option)
Life long immunosuppressants.
Risks of surgery.
Not enough kidneys - may have to wait forever.
What is 4 structures may be damaged in glomerulonephritis?
Capillary endothelium,
Glomerular basement membrane,
Mesangial cells,
Podocytes.
What is NephrOtic Syndrome?
What is the most common sign of this?
Podocyte damage leading to glomerular charge-barrier disruption.
Causes massive proteinuria and oedema.
What triad of signs characterises nephrotic syndrome?
Proteinuria (>350mg/mmol),
Hypoalbumianaemia,
Oedema.
(Also often high cholesterol)
How does diabetic nephropathy occur?
Glycated proteins at the efferent arteriole lead to hyaline atherosclerosis and decreased perfusion, activating RAAS. Mesangial cells over time secrete mor matrix which thickens the basement membrane, decreasing GFR.
How is diabetic nephropathy managed?
Treatment of hypertension and control of glycaemic index. ACEi, ARB
What is minimal change disease?
Autoimmune process resulting in fusion of podocyte foot processes. Named as no significant renal change on light microscopy. Common cause of nephrotic syndrome in children under 6
What is membranous glomerulonephritis?
Subepithelial deposition of immune complexes leading to thickening of the basement membrane. Treated via immunosuppressants and managing underlying causes.
What are the causes of Focal Segmental Glomerulosclerosis?
Primary: idiopathic.
Can be secondary to sickle cell disease, HIV, heroin abuse, kidney hyper perfusion.
What is FSGS
Damage of podocytes and protein buildup in glomerulus, leading to hyalinosis and sclerosis. Treated via steroids.
How is nephrotic syndrome broadly managed?
Diuretics for oedema,
ACEi for proteinuria,
Lifestyle changes to reduce cholesterol,
Treatment of underlying condition eg steroids.
What triad is commonly found in Nephritic syndrome?
Haematuria,
Reduced GFR (presenting as oliguria)
Hypertension.
What is Bergers disease (IgA nephropathy)?
Hypertension and raised IgA levels leading to deposition in the mesangium. Sclerosis of damaged segments. Managed by antihypertensives and steroids.
What is rapidly progressive glomerulonephritis?
Severe glomerular injury due to leakage of fibrin and macrophage/epithelial proliferation. Causes loss of renal function on days to weeks. Treated with steroids, immune suppressants and plasma exchange.
What is GoodPastures syndrome?
Antibodies to type IV collage. build up in glomerular basement membrane and lead to rapid progressive glomerulonephritis, acute renal failure and lung haemorrhage. Treated with plasma exchange and corticosteroids.
What is post streptococcal glomerulonephritis?
Occurs after infection of group A beta haemolytic strep at pahrynx, tonsils or skin. May migrate to kidney. Treated with antibiotics.
How is nephritic syndrome treated?
ACEi or ARBs, Diuretics for oedema, Immune suppressants, Cardiovascular risk management (eg stopping smoking), Dialysis if required (short term).
