Renal Flashcards
AKI
Sudden decline in renal function over hours or days
AKI aetiology
1) pre-renal - renal hypoperfusion
-Reduced circulating volume
-Reduced CO
-Systemic vasodilation
-Arteriolar changes (eg. ACEi/NSAID use)
2) intrinsic renal - structural damage
-Vasculature - atherosclerosis, thromboembolic disease, renal artery stenosis
-Glomerular
-Tubulointerstitial - damage to renal parenchyma that can lead to scarring and fibrosis
–ATN
3) post-renal - results from obstruction (obstructive uropathy)
-Urinary stones
-Malignancy
-Strictures
-BPH
AKI pathophysiology (ATN)
Failure of adequate renal perfusion results in ischaemia
Causes a pro-inflammatory response with the release of cytokines, oxygen free radicals, activations of leucocytes & coagulation pathways (at this point if renal perfusion is not restored, it can lead to cellular injury)
Tubular cells are susceptible due to limited blood supply & high metabolic demand - damaged TCs slough off into the lumen as obstructive casts
Following restoring of normal GFR - kidneys may recover & tubulointerstitial cells regenerate - polyuric phase due to failure of adequate reabsorption by recovering tubules
AKI pre-renal clinical features
Reduced CRT
Dry mucous membranes
Reduced skin turgor
Thirst
Dizziness
Reduced urine output
Orthostatic hypotension
AKI intrinsic renal clinical features
Features of nephritic syndrome - hematuria, proteinuria, oliguria & hypertension
Features of nephrotic syndrome - heavy proteinuria, hypoalbuminaemia & oedema
Tubulointerstitial disease - arthralgia, rashes & fever
AKI post-renal clinical features
Urinary stones - loin to groin pain, haematuria, nausea & vomiting
Prostatic problems - dysuria, frequency, terminal dribbling, hesitancy
Obstruction at bladder neck - palpable bladder, tender suprapubic area
AKI investigations
Assess current fluid status - urine output chart
Bedside - urine dipstick, urine microscopy, urine osmolality & electrolytes, ECG
Bloods - FBC, U&Es, bone profile, blood gas (others can be completed to look for cause of AKI)
Imaging - kidney USS, CXR, renal dopplers, MRA (magnetic resonance angiography)
AKI diagnostic criteria
Serum creatinine
-Stage 1: >/= 26.5 umol/L OR >/= 1.5-1.9 times baseline
-Stage 2: >/= 2.0-2.9 times baseline
-Stage 3: >/= 353 umol/L OR 3 times baseline OR on RRT
Urine output
-Stage 1: <0.5ml/kg/hr for 6-12 hours
-Stage 2: <0.5ml/kg/hr for >/= 12 hours
-Stage 3: <0.3ml/kg/hr for >/= 24 hours OR anuria for >/= 12 hours
AKI management
Guided by the underlying cause
Regular assessment and monitoring
-Monitoring of urine output
-Baseline creatinine & serial U&Es taken daily
-Nephrotoxic drugs should be stopped
Volume dysregulation
-Hypovolaemic - IV fluids
-Hypervolaemic - fluid restriction +/- diuretics
Hyperkalaemia - 10ml of 10% calcium gluconate, insulin and beta agonists
Metabolic acidosis - use of sodium bicarbonate/dialysis
AKI complications
Hyperkalaemia
Fluid overload
Metabolic acidosis
Uraemia
CKD
The presence of kidney damage/reduced kidney function for three or more months
CKD aetiology
Hypertensive nephropathy
Diabetic nephropathy
Glomerulopathies
Inherited kidney disorders
Ischaemic nephropathy
Obstructive uropathy
Tubulointerstitial diseases
Medications
CKD pathophysiology
Renal disease leads to a progressive loss of nephrons and subsequent reduction in GFR
As disease progresses, structural abnormalities may occur leading to kidney damage
Eventually, the kidneys start to lose their ability to carry out normal functions
CKD symptoms
Anorexia & nausea
Fatigue & weakness
Muscle cramps
Pruritus
Dyspnoea
Oedema
CKD signs
Pallor
Hypertension
Fluid overload
Skin pigmentation
Excoriation marks
Peripheral neuropathy
CKD investigations
Urine - urine dipstick, microscopy, ACR (spot & 24-hour collection), electrophoresis
Bloods - FBC, U&Es, bone profile, PTH, bicarbonate, LFTs, lipid profile, autoimmune screen, myeloma screen
Imaging - renal USS, MRA, echo, ECG
Renal biopsy
CKD diagnostic criteria
G1 = GFR > 90
G2 = GFR 60-89
G3 = GFR 45-59 (A), GFR 30-44 (B)
G4 = GFR 15-29
G5 = GFR < 15
A1 = ACR < 3
A2 = ACR 3-30
A3 = ACR > 30
CKD management
Renoprotective therapy - centred around BP control and reducing proteinuria
-Standard BP target for patient with CKD is < 140/90 mmHg
-Pharmacological - ACEi/ARB, SGLT-2 inhibitor, statin therapy, antiplatelets for secondary prevention of CVS disease
Treating complications
-Anaemia - erythropoietin stimulating agents (not recommended until iron-deficiency has been managed)
-Hyperkalaemia - low potassium diets, potassium-binding resins and correction of acidosis
-Mineral and bone disorders
–Hypocalcaemia - dietary supplements and calcitriol
–Hyperphosphataemia - dietary restriction & phosphate binders
–Hyperparathyroidism - calcimimetics/surgery
-Fluid overload - fluid restriction, reduced sodium intake, oral diuretics
-Acidosis - oral sodium bicarbonate therapy
CKD complications
Anaemia
Mineral and bone disorders
Hyperkalaemia
Fluid overload
Acidosis
CKD RRT
Haemodialysis - removal of waste products and other substances by passing blood through a dialysis machine
Peritoneal dialysis - using the peritoneal cavity as the primary site of ultrafiltration
Renal transplant - gold standard for RRT, requires the use of long-term immunosuppressive therapy
Diabetic nephropathy pathophysiology
Chronic high level of glucose passing through the glomerulus causes scarring
Diabetic nephropathy management
Optimising blood sugar levels and BP
ACEi should be started in patients with diabetic nephropathy even if they have a normal BP