RENAL: Acute Renal Disease Flashcards
Define AKI
- Abrupt decline in renal function
- Clinically manifesting as a reversible acute increase in nitrogen waste products, measured by blood urea nitrogen (BUN) and serum creatinine levels - over the course of hours to weeks
How is eGFR calculated?
Mathematically derived based on patient’s serum creatinine lvls, age, sex and race
Usually calculated by lab analysing blood sample, reported with serum creatinine result
“Normal” GFR is usually >90 ml/min/1.73m2. (Note the correction for body surface area “per 1.73m2” which is important for certain patient groups, e.g. amputees, extremes of body habitus.)
What are the limitations of eGFR?
Creatinine-based estimating equations not recommended for use with:
- Individuals with unstable creatinine concentrations
- Pregnant women
- Patiens with serious co=morbid conditions
- Hospitalised patients (particularly those with ACF) Creatinine-based estimating equations should only be used for those with stable concentrations
- Persons with extremes in muscle mass and diet. Includes, but not limited to, individuals who are amputees, paraplegic, bodybuilders, obese, patients with muscle-wasting disease, neuromuscular disorder, suffering from malnutrition, veggie, low-meat diet, or taking creatine dietary supplements
Describe the KDIGO criteria
Stage 1 - Serum creatinine (SCr): 1.5 times baseline or ≥ 26.5micromol/L increase. Urine output: <0.5 mL/kg/h for 6 -12 hours
Stage 2 - Serum creatinine: 2 to 2.9 times baseline. Urine output <0.5 mL/kg/h for 12 hours
Stage 3 - Serum creatinine 3 times baseline OR increase in SCr ≥ 26.5micromol/L to ≥ 354 micro mol/L OR imitation of renal support irrespective of stage OR patients <18 years, decrease in eGFR to <35 mL/min/1.73sqaured. Urine output: <0.3 mL/kg/h for ≥ 24h OR anuria for ≥ 12 hours
Describe the staging of AKI
Pre-renal:
Due to inadequate renal perfusion -ECF volume depletion (e.g. dehydration, sepsis)
Typically do not cause permanent kidney damage, hence potentially reversible, unless hypoperfusion severe and/or prolonged
- Hypovolaemia
- Haemorrhage
- Diasrrhoea/vomiting
- ⬇️Perfusion
- Septic shock
- Cardiac failure
- Drugs
- ACEi
- NSAID
Intrinsic renal disease (renal):
- Glomerular
- Vascular
- Tubular
- Interstitial
Post-renal:
Sudden obstruction of urine flow causing hydronephrosis, hydroureter due to:
- Kidney stones
- Bladder tumour
- Enlarged prostate (men)
Describe intrinsic renal pathology
- Renal causes of AKI involve intrinsic kidney disease or damage. Disorders may involve blood vessels, glomeruli, tubules, interstitium. Most common causes are:
- Acute tubular necrosis
- Acute glomerulonephritis
- Nephrotoxins (including prescription and OTC)
- Glomerular disease increases glomerular capillary permeability to proteins and RBCS; it may be inflammatory (glomerulonephritis) or the result of vascular damage due to ischaemia or vasculitis
- 4 principles - Nephrotic syndrome, nephritic syndrome, isolated proteinuria/haematuria, rapidly progressive GN
- Tubules also may be damaged by ischaemia and may become obstructed by cellular debris, protein or crystal deposition, and cellular or interstitial oedema
- Interstitial inflammation (nephritis) usually involves an immunologic or allergic phenomenon. These mechanisms of tubular damage are complex and interdependent
Describe nephrotic syndrome
- Traingle of oedema, heavy proteinuria (>3.5g/day), hypoalbuminaemia (<30g/L)
Therefore causes all of the following 3: Frothy urine, hypercoagulability, hypercholesterolaemia
Causes:
- Minimal change disease
- Membranous nephropathy
- Focal segmental glomerulosclerosis
Describe rapidly progressive GN
- Like nephritic syndrome but days - weeks
- 3 main groups:
- Anti-glomerular basement membrane (Goodpasture) disease
- Small vessel anti-neutrophil cytoplasm antibody (ANCA) +ive vasculitis
- Miscellaneous conditions >tuft damage> fibrin in Bowman’s capsule
Describe post renal AKI
- Postrenal AKI (obstructive nephropathy) due to various types of obstruction in voiding and collecting parts of urinary system. Obstruction can also occur on microscopic level within tubules when crysatlline or proteinaceous materal precipitates
- Obstructed ultrafiltration, in tubules or more distally, increases pressure in the urinary space of glomerulus, reducing GFR
- To produce significant AKI, obstruction at level of ureter requires involvement of both ureters unless patient has only single functioning kidney
- Bladder outlet obstruction due to enlarged prostate probs most common causes of sudden, and often total, cessation of urinary output in men
How is AKI investigated?
- Bloods
- Urine dip
- BP
- ECG
- Ultrasound
- X-ray
- Labs
How is AKI managed?
- Immediate treatment of pulmonary oedema + hyperkalaemia
- Dialysis needed to control hyperkalaemia, pulmonary oedema, metabolic acidosis, uremic symptoms
- Adjustment of drug regimen for degree of renal dysfunction and stopping offending drug or nephrotoxic (non steroidals)
- Restriction of water, sodium, phosphate, potassium intake, but provision of adequate protein
- Possibly phosphate binders (for hyperphosphatemia) and intestinal potassium binders (hyperkalaemia)
Describe the importances of urine dips and urinary abnormalities
RBC casts and dysmorphic RBCs indicates glomerulonephritis or vasculitis, rarely may occur in acute tubular necrosis
Urinary esoinophils may indicate allergic tubulointerstitial nephritis
With renal tubular injury, seiment characteristically contains tubular cells, tubular cell casts, many granular casts (often with brown pigmentation)
Describe acute tubular injury
Urine output may have 3 phases:
- Prodromal phase - Normal urine output (normally) and varies in duration depending on causative factors (e.g. amount toxin ingested, duration + severity of hypertension etc)
- Oliguric phase - Urine output typically b/w 50 and 500 mL/day. Duration of this phase unpredicatable, depends on etiology of AKI and time to treatment. However, many patients are never oliguric. Nonoliguric patients have lower mortality + morbidity and less need for dialysis
- Postoliguric phase - Urine output gradually returns to normal, but serum creatinine and urea levels may not fall for several more days. Tubular dysfunction may persist for a few days or weeks and is manifested by sodium wasting, polyuria (possibly massive) unresponsive to vasopressin, or hypercholeremic metabolic acidosis
Describe a renal profile
- Urea (2.5-7.8)
- Creatinine ( 60-106 micromol)
- Sodium (133 - 146)
- Potassium (3.5 - 5.3)
- Bicarbonate (22-29)
- eGFR (>90 mls/min)
All units bar creatinine and eGFR are mmol/L
What are the 4 principles of glomerular disease?
- Nephrotic syndrome
- Nephritic syndrome
- Isolated proteinuria/haematuria
- Rapidly progressive GN
Describe nephritic syndrome
Abrupt onset of:
- Haematuria
- Proteinuria
- Decreased GFR (raised creatinine, oedema, hypertension)
Classical cause: Post-streptococcal GN
