Block 4: AKI Flashcards
Continuous renal support
- For very haemodynamically unstable patients that are moved to the intensive care department. Normally a gentle type of dialysis
- Continuous venovenous haemodialysis (CVVHD)
- Continuous venovenous haemofiltration (CVVHF)
- Continuous venovenous haemodiafiltration (CVVHDF)
Complications of AKI- concise
- Fluid overload: leg oedema, pulmonary oedema, pleural effusion
- Electrolyte derangement: hyperphosphatemia, hyperkalaemia
- Acid-base balance: metabolic acidosis
- End organ complications of uraemia
- CKD
- End stage renal disease
When to check PSA and causes of raised lactate
Best to check PSA before inserting a catheter
Causes of raised lactate: reduced organ perfusion/sepsis, metformin use
Post obstruction diuresis (POD)
- A polyuric state where lots of salt and water are eliminated after relief of a urinary tract obstruction.
- Generally occurs after relieving bladder outlet obstruction (BOO), bilateral ureteric obstruction, or unilateral ureteric obstruction in a solitary kidney.
- Diuresis resolves once homeostasis is achieved. These patients are at risk of severe dehydration, electrolyte imbalances, hypovolemic shock, and even death if fluid and electrolyte replacement is not initiated. Can cause ongoing AKI
Pulmonary renal syndrome (PRS)
- Diffuse alveolar haemorrhage plus glomerulonephritis often occurring simultaneously.
- Almost always due to an autoimmune disorder.
- Diagnosis by serology tests and sometimes lung and renal biopsy.
- Treatment includes immunosuppression with corticosteroids and cytotoxic drugs
- Not a specific disease but a syndrome that suggests a differential diagnosis
- Causes: Connective tissue disorder (RA, SLE, Progressive systemic sclerosis), Goodpasture’s syndrome, Renal (IgA nephropathy, idiopathic immune complex glomerulonephritis), Systemic vasculitis (Microscopic polyangitis), drugs, heart failure
Goodpasture’s disease
- Diagnosis: anti-GBM antibodies in the blood or kidney
- Targets the collagen on the basement membrane of alveoli and glomeruli
- It is a rare form of vasculitis that affects the small blood vessels in the kidneys and lungs
- Treatment is with plasma exchange with prednisolone and cyclophosphamide
- If treated quickly good recovery, unlikely to relapse though smoking is a trigger
- If patients on dialysis kidney transplantation is possible when anti-GBM antibodies are undetectable
Rhabdomyloysis
Muscle break down, myoglobin enters the blood stream, goes through the kidneys causing coca-cola urine. In muscle breakdown ATP is depleted causing increased calcium and the generation of free oxygen radicals. This damages the myofilament of the muscle causing increases potassium, phosphate, CK, urate and myoglobin which damage the kidneys
Preventing AKI
- Treatment with IV fluids: fluid resuscitation with 0.9% sodium chloride at a rate of 10-15ml/kg/hr to achieve high urinary flow rates (>100ml/hr), with the cautious addition of sodium bicarbonate 1.4% to maintain urinary pH> 6.51.
- Regular monitoring of U&E’s and CK
- Monitor fluid status to avoid overload
Medications in AKI
- Safe to continue: paracetamol, warfarin , statin (not with rhabdomyolysis), asprin, clopidogrel, beta-blockers
- May worsen renal function: NSAID’s, Aminoglycosides, ACEi, ARB’s, diuretics
Features suggesting CKD not AKI
- Bilateral small kidneys: exceptions are autosomal dominal polycystic kidney disease, diabetic nephropathy, amyloidosis, HIV associated nephropathy
- Hypocalcaemia- due to lack of vitamin D
Kidney- medication
- NSAID’s impair renal autoregulation by inhibiting prostaglandin mediated vasodilation of the afferent arteriole Reduced blood supply through the kidney
- ACEi and ARB’s: reduce systemic blood pressure and also vasodilation of the efferent arteriole. This impairs renal autoregulation and reduced glomerular perfusion pressure.
- If you combine ACi and NSAID’s you would have a lack of blood going in and excess blood leaving, starving the glomerulus of blood
Kidney- Metformin
- Associated with increased risk of lactic acidosis in high risk patients
- Review the dose of metformin if eGFR is below <45
- Stop metformin if eGFR is <30
- Prescribe metformin in caution with rapid change in GFR
- Sulfonylurea increases risk of hypoglycaemia with kidney damage, drug is renally cleared
Kidney- Trimethoprim
Increases risk of hyperkalaemia. Interferes with tubular creatinine secretion causing a rise in creatinine levels and may cause a false positive AKI diagnosis.
AKI definition
An acute rise in creatinine or sustained reduced urine output. Causing failure to maintain fluid, electrolyte and acid-base homeostasis.
Kidney function
1) Excrete water soluble waste products of metabolism
2) Control electrolyte balance
3) Control water volume and balance
4) Control the acid/base balance of the blood
5) Control blood pressure: Through water and electrolyte balance And production of renin
6) Needed for the production of active vitamin D
7) Maintaining haemoglobin through the production of erythropoietin
Inner structure of the kidney
- The kidneys lie retroperitoneally: at vertebral level T12-L3, they are 10-12cm in bipolar length
- The kidneys are surrounded by a tough capsule, and an outer cortex and an inner medulla
- Nephrons in the cortex and medulla filter waste products from the blood, forming urine.
- The pyramids of the cortex drain this into the minor calyces.
- 2-3 minor calyces drain into each of the 2-3 major calyces.
- The major calyces drain into the renal pelvis, which empties through the ureters into the bladder.
Blood flow in the kidneys
- Afferent arteriole supplies blood to the glomerulus: some of it is filtered into the Bowmans capsule
- The filtered blood leaves via the efferent arteriole and divides to form the peritubular capillary network
GFR
- Driven by hydrostatic pressure, oncotic pressure and permeability of glomerular basement membrane (podoctes)
- Approximately 130ml/min/1.73min men and120ml/min/1.73min women
- Begins to decline from 26 years
Role of different parts of the nephron
- Proximal tubule: reabsorbs water, sodium , potassium, bicarbonate, glucose, amino acids. Waste products secreted are creatinine and uric acid
- Loop of Henle: concentration gradient is made through sodium reabsorption allowing urine to be concentrated. Loop diuretics act here. Furosemide acts on the ascending limb
- Distal tubule: re-absorbs sodium, Thiazide diuretics act here
- Collecting duct: reabsorbs some sodium, acid secretion is performed by alpha intercalated cells. ADH acts here inserting aquaporins concentrating urine
Endocrine function of the kidneys
- Vitamin D and renal bone disease: secondary hyperparathyroidism occurs early in CKD. In the kidneys Vitamin D is transformed to its biologically active form
- Kidney regulates calcium and phosphate metabolism through Parathyroid hormone (PTH), calcitriol (1,25 dihydroxycholecalciferol) and calcitonin. Disregulation of calcium and phosphate is a common consequence of CKD which can cause mineral bone disease (CKD-MBD)
- EPO: made by kidneys, prompts bone marrow to make RBC. Treat with erythropoietin stimulating agent (ESA’s) to correct anaemia
Anaemia is defined as
- Females - haemoglobin (Hb) <11.5 g/dL
- Males - Hb <13.0 g/dL
Why is creatinine not the most accurate measure of GFR
It is moderately secreted by renal tubules so slight overestimate. Inulin is more accurate but only used in research.
Parathyroid hormone release is stimulated by a fall in serum calcium
Diseases which can cause an AKI/nephrotic syndrome
Diseases with can cause an AKI: SLE, vasculitis, infection (hepatitis B/C, HIV), myeloma
Diseases which can cause nephrotic syndrome (heavy proteinuria): Diabetes, SLE, amyloid, infection (Hep B/C, HIV), Myeloma
Common illness’s prior to kidney damage
- Pharyngitis – IgA nephropathy or post-streptococcal glomerulonephritis
- Vomiting/ diarrhoea/ blood loss – predispose to volume loss and pre renal failure
- Sepsis – risk factor for pre-renal failure/ ATN
- Back pain – myeloma
Causes of polyuria
- Diuretic agents
- Reduced ADH secretion (Cranial diabetes insipidus, alcohol)
- Insensitivity to ADH (nephrogenic diabetes insipidus)
- Psychogenic polydipsia
- Atrial naturitic peptide (ANP) release – e.g cardiac arrhythmias, cardiac failure
- Osmotic diuresis (hyperglycaemia, hypercalcuria)
- CKD – inability of diseased tubular cells to appropriately move sodium and hence concentrate urine
Other causes of urinary symptoms
- Nocturia: CKD, diabetes, prostatic disease
- Increased urinary frequency: diabetes, hypercalcuria, UTI
- Poor urinary stream: prostatic disease or sphincter dysfunction
- Dysuria (pain): UTI or urethritis (gonococcal infection)
Causes of different urine colour
- ‘Cola coloured’ – Nephritic syndrome (where there is glomerular haematuria)
- ‘Tea coloured’ – due to myoglobinuria, usually secondary to rhabdomyolysis.
- Macroscopic haematuria – bleeding in upper urinary tract (e.g IgA nephropathy)- bleeding in lower urinary tract (e.g bladder cancer, renal calculi)
- Frothy – heavy proteinuria (nephrotic syndrome)
- Orange to Pink-red (Rifampicin or beetroot ingestion)
- Bright/ strong yellow – cholestatic jaundice
- Discolouration of urine on standing – alkaptonuria, porphyria
Other symptoms of kidney damage
- Loin pain: kidney stones, infection, IgA nephropathy, polycystic kidney disease. Renal colic (due to kidney stones) agonising requires opiated
- Oedema: occurs in fluid overload or in nephrotic syndrome where heavy proteinuria leads to reduced oncotic pressre
- Symptoms of hypertension: headache, blurred vision
- Symptoms of anaemia: tiredness, dyspnoea
- Symptoms of uraemia: nausea, vomiting, chest pain associated with pericarditis or confusion
- Symptoms of hyper-phosphataemia: itchiness, lethargy
CKD definition
Abnormalities of kidney function or structure present for more than 3 months. The definition of CKD includes all individuals with markers of kidney damage or those with an eGFR of less than 60 ml/min/1.73m2on at least 2 occasions 90 days apart (with or without markers of kidney damage).
Markers of kidney dysfunction
Albuminuria (ACR > 3 mg/mmol), haematuria, electrolyte abnormalities due to tubular disorders, renal histological abnormalities, structural abnormalities detected by imaging or a history of kidney transplantation.
Causes of CKD
- AKI which does not recover
- Glomerular disease
- Systemic disease: diabetes, hypertension, autoimmune
- Vascular: renovascular or thrombotic disease
- Reflux nephropathy: Drugs/toxins
- Inherited: Polycycstic kidneys, Alports syndrome
- Post obstructive causes
CKD investigations with blood results
- Urine: volume, dipstick and microscopy
- Urine albumin and protein quantification using ACR or PCR
- Bloods: FBC, U&E, LFT, bone profile, blood culture, immunology
- Blood results: Hyperparathyroidism, iron deficient anaemia, Hypocalcaemia, Hyperphosphataemia, vitamin D deficiency
- Kidney biopsy is the gold standard
CKD therapeutic targets
- Control of blood pressure and proteinuria
- This will reduce the rate of decline in GFR and reduce cardiovascular risk
CKD can be characterised by one or more of the following markers
- Albuminuria (e.g. albumin:creatinine ratio > 3 mg/mmol or > 30 mg/g)
- Urinary sediment abnormalities (e.g. white cell or red cell casts)
- Radiological abnormalities (e.g. polycystic kidneys)
- Pathological abnormalities (e.g. seen on renal biopsy)
- Kidney transplantation
The definition of CKD is the presence of either of the following for 3 months or more
- Albuminuria (> 3 mg/mmol, i.e. A2/3)
- Abnormalities (including electrolyte derangement) secondary to tubular disorders
- Structural abnormalities
- Abnormalities on histology
- History of kidney transplant
- Reduced GFR: GFR < 60 ml/min/1.73 m2 (i.e. G3a-G5)
What is CKD classified on
Cause, GFR category (G1-G5) and Albuminuria category (A1-A3)
CKD- GFR categories
- G1: Normal or high: >90
- G2: mildly decreased: 60-89
- G3a: mildly to moderately decreases: 45-59
- G3b: moderately to severely decreased: 30-44
- G4: severely decreased: 15-29
- G5: kidney failure : <15 or on dialysis
CKD: Albuminuria categories (albumin:creatinine ratio)
- A1: normal to mildly increases (<3 mg/mmol)
- A2: moderately increased (3-30 mg/mmol)
- A3: severely increased (>30 mg/mmol)
CKD: creatinine
If creatinine is above >90ml/min/1.73 its assumed normal function. Though if there has been structural or function damage for >3 months can still diagnose. IF GFR <60 ml/min for 3 months can assume kidney disease is present
End stage renal disease: if GFR is <15 or the patient is on dialysis. eGFR is a blood test
Monitoring CKD
- Requires a FBC and iron studies (for anaemia), serum calcium, phosphate and parathyroid hormone levels (for renal bone disease)
- Low-moderate risk: monitor annually
- High risk: monitor every 6 months
- Very high risk: monitor every 3-4 months
Complications of CKD
- Salt and water balance: hypertension, oedema, heart failure
- Potassium balance: Hyperkalaemia
- Elimination of nitrogenous wate: uraemia (pericarditis, reduced immune function, sexual dysfunction, GI and neurologic manifestations, coagulopathies (bleeding)
- Erythropoietin production: anaemia
- Acid-base balance: acidosis
- Activation of vitamin D: Hypocalcaemia
- Phosphate elimination: Hyperparathyroidism
Causes of CKD
- Multisystem disease with renal involvement: SLE, vasculitis, myeolma, hepatitis B/C, HIV
- Hereditary kidney disease: polycystic kidney disease, Alport syndrome
- Glomerular disease: IgA nephropathy, membranous nephropathy, focal segmental glomerulosclerosis
- Nephrotoxic drugs: lithium, PPI, NSAID, bisphosphonates
- Obstructive uropathy: benign prostatic hypertrophy, urinary tract calculi, malignancy, fibrosis
- Most common: diabetes, hypertension and vascular disease
Symptoms of CKD and GFR with age
GFR with age: after a peak at 26 there is a an annual decline of 1ml/min/year.
Symptoms
- Normally asymptomatic, symptoms start to develop in stages 4-5
- Normally detected through the presence of hypertension, haematuria and/or proteinuria upon urinalysis or a reduction in GFR with increased serum creatine
- General symptoms: such as fatigue, nausea and vomiting, cramps, insomnia, restless legs, taste disturbance, bone pain, and pruritus
- Abnormal urine output: such as polyuria, oliguria, or nocturia
- Fluid overload: raised JVP, dyspnoea and orthopnoea
- Sexual dysfunction, skin pigmentation and excoriation marks
- Severe uraemia may also cause hiccups, pericarditis, coma and seizures
Typical clinical findings in CKD
- Uraemic fetor: ammonia-like smell of the breath
- Pallor: due to anaemia
- Cachexia
- Cognitive impairment: specifically affecting language, orientation andmattention
- Tachypnoea: may be due to fluid overload, anaemia
- Hypertension
- Volume disturbance: volume overload (e.g. peripheral oedema, pulmonary oedema, pleural effusions, ascites) or volume depletion
- Peripheral neuropathy
- Fundoscopy may reveal microvascular damage in patients with diabetes or hypertension
Specific clinical findings depending on underlying cause of CKD
- Bilateral masses upon palpation of flanks, suggestive of adult polycystic kidney disease. May be accompanied by hepatomegaly due
to liver cysts. - Palpable bladder: may suggest obstructive uropathy, often accompanied by prostatic enlargement in men
CKD: investigations
- Urine: urine dipstick, urine microscopy, ACR (spot test), ACR (24 hour collection), Electrophoresis (i.e. myeloma)
- Bloods: FBC, U&E (inc eGFR), Bone profile, PTH, bicarbonate, LFT’s, lipid profile, Autoimmune screen (ANCE, ANA), myeloma screen
- Imaging: Renal ultrasound, Magnetic resonance angiography, Echocardiogram, ECG (high risk of CVS disease), Renal biopsy (for intrinsic causes)
CKD: when should a renal ultrasound be offered
A renal ultrasound scan should be offered to patients with visible or persistent non-visible haematuria, evidence of obstructive uropathy, family history of PCKD, reduced eGFR (< 30ml/min) or accelerated progression of CKD.
General measures for the management of CKD include
- Exercise
- Healthy weight loss
- Smoking cessation
- Good glycaemic control
- Control of blood pressure
- Immunisations: influenza and Pneumococcus
- Avoidance of nephrotoxic medication
- Diet: adequate protein intake, restricted sodium and phosphate intake
- Plan for RRT
- Cardiovascular disease prevention: assess for cardiac risk factors - offer statin
CKD and hypertension
- In adults with CKD and an ACR under 70 mg/mmol, aim for a clinic systolic blood pressure below 140 mmHg (target range 120 to 139 mmHg) and a clinic diastolic blood pressure below 90 mmHg.
- In adults with CKD and an ACR of 70 mg/mmol or more, aim for a clinic systolic blood pressure below 130 mmHg (target range 120 to 129 mmHg) and a clinic diastolic blood pressure below 80 mmHg.
- In patients with significant proteinuria use an ACEi or ARB
CKD: offer an ACEi or ARB if
- Diabetic and have an ACR ≥ 3 mg/mmol (even in the absence of
hypertension) - Hypertensive and ACR > 30 mg/mmol
- ACR > 70mg/mmol (even in the absence of hypertension)
