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UG renal pathophysiology summary
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Summary of lectures 3-6 renal pathophysiology.
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UG Key Summary Notes:1. Chronic Kidney Disease (CKD):
Definition: CKD is defined by the presence of 1 or more markers of
kidney damage (Albuminuria, Urinary sediment abnormality,
electrolyte or other abnormality due to tubular disorder,
abnormalities on histology, structural abnormalities noted on
imaging, h/x of a Kidney transplant) or decreased kidney function
(eGFR < 60mL/min per 1.73m3) or both for >/= 3 months
irrespective of the cause
Epidemiology: 14th leading cause of death (12.2 deaths per 100,000)
Predict it will increase to 14 per 100,000 by 2030
Complications: - Non-excretory function of kidneys 1.
Normocytic/Microcytic Renal Anaemia (EPO deficiency – most sig.
mechanism, increased microscopic blood loss in gut, bone marrow =
dec. RBC prod.= uraemic toxins, Haematinic deficiency iron/vit.
Deficits, increased RBC destruction = due to decreased half-life, ACE
Inhibitors interference in EPO regulation in kidneys) & 2. CKD-MB
(CKD-Mineral and Bone disorder) / Hyperparathyroidism (decreased
alpha-1 hydroxylase = decreased conversion to 1,25-dihydroxy-
vitamin D3 (active) degree of bone demineralisation + reduced
absorption of Ca2+ in gut = increased PO43- = PT stimulated
Increased PTH = low Ca2+ detected in blood secondary
hyperparathyroidism)
Aetiology/causes: 70% of CKD is caused by 3 main drivers = 1.
Diabetes Secondary glomerular disease (diabetic
glomerulosclerosis – in diabetic nephropathy), 2. Hypertension
(Hypertensive nephrosclerosis), 3. Renovascular disease
Management / Treatment: Dialysis/RRT for early-stage CKD, manage
CVS risk 1. Lifestyle change (modify diet for raised phosphate -
, either recommend reduced phosphate diet or GI phosphate binders
with each meal), weight loss, smoking cessation 2. tight BP control &
DM control 3. Ptx’s with proteinuria = RAAS blockade + Na-Glu co-
transporter 2 inhibitors (SGLT2i- diabetes management) 4. Iron
prescribed for anemia + EPO (IV/SBC) = correct Hb level.
Pathophysiology: Damage caused by either systemic hypertension
&/ intraglomerular hypertension and as a consequence, initially get
glomerular hypertrophy as an adaptive process further damage of
local tissue with epithelial/ endothelial cell injury leads to
proteinuria => Extravasation of proteins into the intraglomerular
space which then causes inflammation + damage
Glomerulosclerosis => reduction in funct. renal cell mass = start cycle
again. Final common pathway = renal fibrosis =
Glomerulosclerosis in glomerulus + tubular atrophy + interstitial
fibrosis in tubular system (if found on biopsy = irreversible kidn.
damage).
Staging: G1, G2, G3a, G3b, G4, G5 eGFR </= 15 mLs
Normal with markers of As soon as eGFR<30 mLs/
kidney dysfunction – eGFR<60mLs/ min on 2
e.g. haematuria/ min & is split consecutive
proteinuria/ confirmed into a & b in occasions =
kidney disease on recognition of advanced CKD
imaging different
prognosis
Take care with: Ptx’s with CKD = subs. Increase in CVS risk + CKD = an
inde. Risk factor for CVS Most likely to die from CVS event before
needing dialysis.
Risk Factors: -Hypertension (+ left. Ventricular hypertrophy),
diabetes, dyslipidaemia, older age, retention of uraemic toxins,
anaemia, elevated levels of certain cytokines, positive calcium
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