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
Nephrotic syndrome
Triad of heavy proteinuria > 3.5g/day, hypoalbuminaemia & oedema
Nephrotic syndrome aetiology
Divided into primary or secondary
Primary
-Minimal change disease
-Focal segmental glomerulosclerosis
-Membranous nephropathy
Secondary
-Diabetes mellitus
-Amyloidosis
-HIV
Minimal change disease pathophysiology
Minimal change disease - fusion of podocyte foot processes under electron microscopy
Suspected to be immune dysfunction that leads to production of a permeability factor that disrupts the filtration barrier
Nephrotic syndrome symptoms
Shortness of breath
Foamy urine - excess protein loss
Fatigue
Poor appetite
Peripheral oedema
Periorbital oedema
Nephrotic syndrome signs
Oedema
Ascites
Effusions
Nephrotic syndrome investigations
Bloods - FBCs, U&Es, LFTs, CRP, lipid profile, clotting profile
Urine - dipstick, microscopy
Imaging - renal USS, CXR
Renal biopsy
Nephrotic syndrome management (MC, FSGS, MN)
Minimal change disease - systemic glucocorticoids (eg. prednisolone)
FSGS - primary = immunosuppressive medications, secondary = treat underlying cause
Membranous nephropathy - primary = immunosuppressive medications, secondary = targets the underlying cause
Nephrotic syndrome complications
Thrombosis - DVT and PE are particularly common
Hyperlipidaemia
Recurrent infections
Acute kidney injury
FSGS pathophysiology
-Primary - circulating factor that damages podocytes leading to foot process effacement (loss of structure -> causing them to spread out & reduce effectiveness of filtration barrier)
-Secondary - adaptive response to renal injury (combination of glomerular hypertrophy & hyperfiltration)
Membranous nephropathy pathophysiology
-Primary - autoimmune reaction against important antigens in the filtration barrier -> development of autoantibodies (against phospholipase A2 receptor)
-Secondary - SLE, viral hepatitis, prostate cancer, NSAID use
Urgent dialysis indications
Uraemic encephalopathy
Hyperkalaemia resistant to medical treatment
Metabolic acidosis uncontrolled by medical treatment
Pulmonary oedema with oliguria
Dialysis
Method for performing the filtration tasks of the kidneys artificially in patients with end stage renal failure or complications of renal failure
Involves removing excess fluid, solutes and waste products
Long term dialysis indications
End stage renal failure (CKD stage 5)
Any of the acute indications continuing long term
Peritoneal dialysis
Uses the peritoneal membrane as the filtration membrane
Special dialysis solution containing dextrose is added to the peritoneal cavity
Ultrafiltration occurs from the blood, across the peritoneal membrane, in to the dialysis solution
Dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution
Tenckhoff catheter – plastic tube that is inserted into the peritoneal cavity with one end on the outside (allows access to the peritoneal cavity, used for inserting and removing the dialysis solution)
Peritoneal dialysis complications
Bacterial peritonitis – infusions of glucose solution make the peritoneum a good place for bacteria to grow
Peritoneal sclerosis – thickening and scarring of the peritoneal membrane
Ultrafiltration failure – occurs when the patients starts to absorb the dextrose in the filtration solution, reduces the filtration gradient making ultrafiltration less effective, becomes more prominent over time
Weight gain – absorb the carbohydrates in the dextrose solution
Psychosocial effects – having to change dialysis solution and sleep with a machine every night
Haemodialysis
Patients have their blood filtered by a haemodialysis machine
Regimes can vary but a typical regime might be 4 hours a day for 3 days a week
Need good access to an abundant blood supply, options are:
1) Tunnelled cuffed catheter
2) Arterio-venous fistula
Tunnelled cuffed catheter
Tube inserted into the subclavian/jugular vein with a tip that sits in the SVC/right atrium
Two lumens – one for blood exiting and one where blood enters
Dacron cuff – surrounds the catheter, promotes healing and adhesion of tissue to the cuff, making it more permanent and providing a barrier to bacterial infection, can stay long term
Main complications – infection and blood clots
A-V fistula
Artificial connection between an artery to a vein (surgical operation and a 4 week to 4 month maturation period without use)
Provides a permanent, large, easy access blood vessel with high pressure arterial blood flow
Typically in patient’s forearm – radio-cephalic, brachio-cephalic, brachio-basilic
A-V fistula examination
Skin integrity
Aneurysms
Palpable thrill (fine vibration felt over the anastomosis)
Stereotypical machinery murmur on auscultation
A-V fistula complications
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output heart failure
STEAL syndrome
Inadequate blood flow to the limb distal to the AV fistula
AV fistula steals blood from the distal limb
Blood is diverted away from where it was supposed to supply and slows straight into the venous system
Causes distal ischaemia
High output heart failure (AV fistula complications)
AV fistula blood is flowing very quickly from the arterial to the venous system through the fistula
Means there is rapid return of blood to the heart -> increases the pre-load in the heart -> hypertrophy of the heart muscle and heart failure
Polycystic kidney disease
Genetic condition where the kidney develop multiple fluid-filled cysts
Kidney function is impaired
Palpable, enlarged kidneys may be felt on examination
Autosomal dominant and recessive type (dominant is more common)
Diagnosis – kidney USS and genetic testing
ADPKD genes
PKD-1 (chromosome 1) is majority
PKD-2 (chromosome 4)
ADPKD extra-renal manifestations
Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cardiac valve disease (MR)
Colonic diverticula
Aortic root dilatation
ADPKD complications
Chronic loin pain
Hypertension
CVD
Gross haematuria
Renal stones
End stage renal failure
ARPKD
Gene on chromosome 6
Rarer and more severe
Often presents in pregnancy with oligohydramnios (fetus does not produce enough urine)
ARPKD features
Oligohydramnios leads to underdevelopment of the lungs resulting in respiratory failure shortly after birth
Patients may require dialysis within the first few days of life
Can have dysmorphic features – underdeveloped ear cartilage, low set ears & flat nasal bridge
Usually have end-stage renal failure before reaching adulthood
PKD management
Tolvaptan (vasopressin receptor antagonist) – can slow development of cysts & progression of renal failure in ADPKD
- Should be initiated and monitored by a specialist
Mainly supportive of complications: anti-hypertensives, analgesia, abx, dialysis, renal transplant
Other: genetic counselling, avoid contact sports, avoid NSAIDs & anticoagulants, regular USS to monitor cysts, regular BP, MR angiogram can be used to diagnose intracranial aneurysms
Donor matching for renal transplant
Matched based on HLA type A, B & C on chromosome 6
Recipients can receive treatment to desensitised them to donor HLA when there is a living donor
Less they match, the more likely the transplant is to fail
Renal transplant procedure
Patient’s own kidneys are left in place
Donor kidney’s blood vessels are connected with the patient’s pelvic vessels, usually the external iliac vessels
Donor kidney’s ureter is anastomosed directly with the patient’s bladder
Placed anterior in the abdomen and can usually be palpated in the iliac fossa area
Typically hockey stick scar
Post renal transplant
New kidney will start functioning immediately
Patients will require life long immunosuppression to reduce the risk of transplant rejection
Usual regime: tacrolimus, mycophenolate, prednisolone
Others: cyclosporine, sirolimus, azathioprine
Renal transplant complications
Relating to transplant – transplant rejection (hyperacute, acute & chronic), transplant failure, electrolyte imbalances
Relating to immunosuppressants – ischaemic heart disease, T2DM, infections more likely & more severe, unusual infections (PCP, CMV, PJP & TB), non-Hodgkin lymphoma, skin cancer (particularly SCC)
