renal essay - chronic kidney disease Flashcards
What is the key difference between the presentations of acute kidney injury and chronic kidney disease?
AKI predominantly causes issues with biochemistry, while CKD has the addition of slowly developing endocrine and metabolic issues
What are the 4 key pathologies in CKD?
anaemia, reduced renal size, renal osteodystrophy, peripheral neuropathy
What are some of the common causes of CKD?
diabetes, hypertension, glomerulonephritis, polycystic kidney disease
What fluid/electrolyte imbalances occur in CKD?
Inability to either concentrate or dilute urine, polyuria/nocturia, Na+ retention or wasting, K+ retention, metabolic acidosis (decreased HCO3 production)
Why does CKD present with anaemia?
Kidneys produce less EPO due to reduced O2 sensing, leading to a low Hb concentration and normochromic & normocytic anaemia.
In addition, chronic inflammation increases hepcidin, reducing iron absorption and recycling.
What are the effects of CKD on metabolic function?
Dyslipidaemia, atherogenesis, abnormal sex hormone/reproduction function
Why is there polyuria in CKD?
Surviving nephrons hypertrophy due to their increased workload, resulting in an increased flow rate for each nephron. The increased flow rate prevents the concentration of urine as the loop of Henle cannot generate HOMG. Plasma osmolarity drops and there will be polyuria unless GFR is very low.
How is sodium homeostasis maintained in the earlier stages of CKD?
Sodium balance is maintained until the later stages of the disease as the increased flow rate causes reduced reabsorption, which increases relative excretion in the urine, compensating for the reduced filtration. In the later stages, wasting or retention may occur
What happens to potassium balance in CKD?
Tends to be K+ retention, resulting in elevated plasma concentration and low urinary concentration
Why does there tend to be a metabolic acidosis in CKD?
There are fewer functioning nephrons making HCO3-, there is decreased ability to secrete ammonium and other acids, and a decreased ability to secrete H+
How is plasma urea maintained at stable concentrations in CKD despite renal impairment?
As renal function declines, there will be a gradual accumulation of urea and creatinine due to low GFR. However, since there will be a higher plasma concentration, filtered load can be maintained despite falling GFR.
What is the management of CKD anaemia?
IV iron therapy, reduction in unnecessary blood tests, EPO therapy until Hb is 110-120
What is the pathogenesis of renal bone disease?
- reduced renal phosphate excretion and vitamin D activation by calcitriol in the kidneys in CKD.
- low calcitriol reduces calcium uptake in the gut
- Parathyroid responds to high phosphate/low calcium and releases parathyroid hormone.
- PTH causes FGF-23 release, which promotes bone remodelling and reduced mineralisation.
- Lack of calcitriol prevents feedback inhibition of PTH, worsening process,
- acidosis causes bone breakdown to generate buffers
What are the clinical findings in renal bone disease?
hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase, ectopic/metastatic calcification in soft tissues, arterial calcification, osteomalacia (spine, etc.)
What is the management of renal bone disease?
Dietary phosphate restriction (low protein), PTH supression with calcitriol, acidosis correction with sodium bicarbonate
