Chronic Renal Failure Flashcards
(30 cards)
Chronic Renal Failure (CKD)
-Progressive kidney failure
-diabetes, hypertension and vascular disorders
-filtration and tubular function decrease
Kidney adapts to CKD
-nephrons hypertrophy and hyperfunction [Maintains filtration, secretion and reabsorption]
-continuing damage will decrease function=glomerulosclerosis
Pathophysiology of CKD Proteinuria
Glomerular hyperfiltration leads
to an increase in glomerular
capillary permeability.
Increase in protein level in
interstitial fluid = tubulointerstitial injury
Pathophysiology of CKD Angiotensin 2
Angiotensin II promotes
glomerular hypertension.
Leads to systemic hypertension.
Clinical Manifestations of CKD
Azotaemia (benign) = build up of creatine and urea do decrease in kidney funtion
Uraemia= pathological build up of nitrogenous waste
Uremic Syndrome
-inflammation, increased nitrogenous compounds= urea, cynate, creatinine
Impacts= glucose tolerance, abnormal lipid metabolism and hyperparathyroidism
Acute Kidney Injury
-abrupt loss of renal function less than 7 days
-5% of hospitalised patients (50-80% die)
-Causes= ischaemia, drugs, hypotension
-Classification of causes= prerenal, intrarenal, postrenal
Prerenal AKI
Most common cause of
AKI.
-Reduced renal blood flow causes renal hypoperfusion.
- Tubuloglomerular
feedback initially
compensates.
Intrarenal AKI
-Disorders involving the tissue of the kidney.
-ischaemia, acute tubular necrosis (ATN) commonly
- surgery 50% of ATN
-Low blood pressure
-active inflammation
-free radicals
Gentamycin=nephrotoxicity
Postrenal AKI
Rare cause of AKI.
Blockages cause an increase in pressure within the kidney.
Hypertension leads to a loss of filtration
Phases of AKI.
3 phases.
-Initiation Phase (24-36 hours)
-Oliguric Phase (can persist for weeks)
-Repair Phase
AKI Consequences
-metabolic acidosis
-hyperkalaemia
-uremia
Diagnosis of AKI
-Increase in serum Creatinine by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours.
-Increase in serum Creatinine to ≥1.5 times baseline in 7 days.
-Urine volume < 0.5 ml/kg/h for 6 hours.
Renal biopsy
-invasive, requires specific indications
-extract sufficient glomeruli for effective diagnosis (20)
Glomerulonephritis
-can be autoimmune
-acute forms= Post-infective.
Rapidly progressive.
Goodpasture’s syndrome
-lupus can give rise to
Post-infective glomerulonephritis
-infection with group A B-haemolytic streptococci = strep pyogenes (7-12days after
-complement and immune infiltration result in loss of kidney function
-symptoms:
Oliguria in initial stage.
Haematuria/proteinuria.
Oedema due to sodium retention
[Anti-C3 antibody staining]
Streptococcus Pyogenes
- gram positive
-normal flora
-scarlet fever, strep throat (opportunistically)
-toxin producing
Erythrogenic Toxins
-cause of post-streptococcal glomerulonephritis
-13 different (SpeA-SpeC)
-SpeB, cysteine protease
enzyme. [cleaves Ig and complement, occasionally leaves anti-complement proteins]
Penicillin
-for strep. pyogenes.
-beta lactam
-inhibits cell wall synthesis peptidoglycan cross linking inhibition
Goodpasture’s syndrome
-aggressive glomerulonephritis
-Abs against glomerular basement membrane
=anti-GBM
=forms of IgG
-genetic HLA-DRB1
Goodpasture’s syndrome on kidney
-80% kidney symptoms
-coughing up blood
-chest pain
-shortness of breath
-lung symptoms before renal
-Anti-GBM Abs target Type 4 collagen
Nephrotic Syndrome
-gross proteinuria (over 3.5g/day)
-hypolbuminaemia
-several damaged glomerular membrane
-IgA nephropathy can cause (men over 30)
Oedema in nephrotic syndrome
-Proteinuria results in
hypoalbuminaemia.
-Intravascular oncotic
pressure drops
compared to interstitial.
-Fluid flows from the
vascular compartment
into the interstitium.
Renal Cancer
Renal tubular cells.
- Adenomas.
- Renal cell.
Renal pelvis.
-Transitional cell carcinoma.
