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10 Cards in this Set

  • Front
  • Back

Causes of CKD

1. AKI


2. Hypertension


3. Diabetes mellitus


4. Other renal problems (eg polycystic kidney disease)



AKI

Reversible


3 types:


Prerenal: renal artery stenosis, heart failure, haemorrhage (all decrease blood flow to kidney and thus decrease GFR)


Renal: glomerulonephritis, tubular necrosis, interstitial nephritis


Postrenal: benign prostatic hyperplasia, kidney stones, tumour




Both prerenal and postrenal AKI can lead to subsequent renal AKI

Hypertension: Mechanism of CKD

1. Hypertension causes thickening of blood vessels which leads to narrowing of lumen


2. In renal arteries this leads to decreased blood flow to kidneys and therefore a decrease in GFR


3. This is detected by JG cells which consequently produce renin leading to the activation of the RAAS


4. This leads to an increase in heart rate and in blood pressure which may restore GFR for a while but eventually will just lead to further vessel wall thickening and a further decrease in GFR


5. This eventually leads to glomerularsclerosis: thickening and hardening of the vessels in Bowman's capsule


6. This leads to ischaemic injury to the nephron and thus nephron loss

Diabetic Nephropathy: Mechanism

1. Hyperglycaemia leads to the increase of reactive oxygen species (ROS) in the blood


2. ROS then leads to the activation and production of unnecessary growth factors, proinflammatory cytokines and leads to an increase in oxidative stress.


3. In the nephron this translates to 4 changes:


- 1. Mesangial expansion and proliferation


- 2. Podocytopathy leading to podocyte hypertrophy and eventual atrophy


- 3. GBM thickening


- 4. Sclerosis

CKD: General Mechanism

1. Loss of nephrons leads to shift in blood flow to those nephrons that are still function leading to glomerular hyperfiltration


2. Early Stage:


There is an increase of GFR in the functional nephron due to increased blood flow however the increased blood pressure this causes leads to glomerularsclerosis which leads to loss of the nephron


3. Late Stage:


So much kidney function is lost that there is a permanent decrease in GFR, urine output and uremia occurs

Clinical Symptoms

1.Na+ balance and H20


2. K+ balance


3. Metabolic acidosis


4. Mineral balance and osteodystrophy


5. Uraemia

Na+ Balance and H20

- A decrease in GFR leads to and increase in Na+ and H20 retention which in turn leads to and increase in BP and peripheral oedema


- To combat this one must restrict fluid intake


- Vomiting and diarrhoea (sudden Na+/H2O loss) very dangerous



K+ balance

Decreased GFR leads to increased K+ retention


This leads to hyperkalemia causing muscle weakness, ECG changes, fibrillations


Loss of nephrons -> decreased renin production which follows on to produce decreased aldosterone which makes the distal Na+/K+ pump nonfunctional leading to further K+ retention


- Use of K+ sparing diuretics and ACE inhibitors further aggrevates problem

Metabolic acidosis

Diminished capacity to excrete H+ and generate HCO3 -> ACIDOSIS


Acidosis -> bone decalcification

Mineral balance and osteodystrophy

Loss of nephrons -> decreased calcitriol