Renal Flashcards
Complications of Nephrotic Syndrome?
Increased risk of VTE, infections, cardiovascular complications, anaemia, acute renal failure and hypovolaemic crisis.
Patients with nephrotic syndrome are at a higher risk of VTE due to the loss of anti-thrombin III. Anti-thrombin III inhibits the action of thrombin and loss creates a pro-coagulant state and therefore prophylactic LMWH is recommended.
Obesity, growth retardation and papilloedema are complications of corticosteroids, which are commonly used in the management of nephrotic syndrome.
Haemorrhagic cystitis is a common complication of cyclophosphamide, another drug used in the management of nephrotic syndrome. However, haemorrhagic cystitis is not a recognised complication of nephrotic syndrome.
Glomerulonephritis causes of Nephrotic syndrome
Minimal change (young people) Membranous GM Focal Segmental Glomerulonecrosis (most common in adults) Amyloidosis Diabetic nephropathy
What are the pre-renal causes of AKI
One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.
Examples
- hypovolaemia secondary to diarrhoea/vomiting
- renal artery stenosis
What are the intrinsic causes of AKI
intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.
Examples
- glomerulonephritis
- acute tubular necrosis (ATN)
- acute interstitial nephritis (AIN), respectively
- rhabdomyolysis
- tumour lysis syndrome
What are the post-renal causes of AKI
An obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function. An example could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by benign prostatic hyperplasia.
Examples
- kidney stone in ureter or bladder
- benign prostatic hyperplasia
- external compression of the ureter
Risk factors for AKI
- chronic kidney disease
- other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
- history of acute kidney injury
- use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, ARBs and diuretics) within the past week
- use of iodinated contrast agents within the past week
- age 65 years or over
- oliguria (urine output less than 0.5 ml/kg/hour)
- neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
Signs of an AKI are
- a reduced urine output. This is termed oliguria and is defined as a urine output of less than 0.5 ml/kg/hour
- fluid overload
- a rise in molecules that the kidney normal excretes/maintains a careful balance of. Examples include potassium, urea and creatinine
Metabolic acidosis with a raised anion gap
- Lactic acid (sepsis, tissue ischaemia)
- Urate (renal failure)
- Ketones (diabetic ketoacidosis)
- Drugs/ toxins (salicylates, methanol, ethylene glycol)
Metabolic acidosis with a normal anion gap
- Renal tubular acidosis
- Diarrhoea
- Addison’s disease
- Pancreatic fistula
- Hyperchloraemia
Staging AKI
- Creatinine x1.5 baseline OR <0.5ml/Kg/hr for 12 hours
- Creatinine x2.0 baseline OR <0.5 ml/Kg/hr for more than 12 hours
- Creatinine x3.0 baseline OR <0.3ml/Kg/hr for more than 24 hours OR Anuria for 12 hours
Drugs which should be stopped in AKI (DAAAMN)
Diuretics Aminoglycosides (Gentamicin) ACE-i ARBs Diuretics Metformin NSAIDs
Minimal change disease
Mainly idiopathic
T-cell and cytokine mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin
Management
majority of cases (80%) are steroid responsive
cyclophosphamide is the next step for steroid resistant cases
Infrequent or frequent relapses in 2/3 patients
haemolytic uraemic syndrome
Thrombocytopenia + Acute renal failure
More common in young children
Causes post-dysentery - E coli 0157:H7 (enterohaemorrhagic) tumours pregnancy Ciclosporin, the Pill Systemic lupus erythematosus HIV
Management
Supportive (fluids, transfusion and dialysis)
Henoch-Schonlein purpura
Overlap with Berger’s disease
Type III (IgA) hypersensitivity reaction
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure
Treatment
- Analgesia for arthralgia
- Treatment of nephropathy is generally supportive.
Alport syndrome
X-linked dominant pattern. Defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).
Usually presents in childhood
Features microscopic haematuria progressive renal failure bilateral sensorineural deafness lenticonus retinitis pigmentosa
Diabetic nephropathy management
Screening - early morning albumin:creatinine ratio
>2.5 = microalbuminurea
Management
- dietary restrcitons + tight glycaemic control
- BP <130/80 mmHg
- ACE-i and ARBs can be used
- Statins
Normal Anion gap
The normal value for the serum anion gap is 8-16 mEq/L
Difference between pre-renal and tubular causes in acute renal failure
Tubular causes affect the fucntion of the nephrons resulting in less Na+ reabsorped so higher Urinary Sodium
in Pre-renal causes, the tubules are working normally so urinary sodium will be low/normal
Cranial Diabetes Insipidus
Causes;
- idiopathic
- post head injury
- pituitary surgery
- craniopharyngiomas
- histiocytosis X
- Wolfram’s syndrome Treatment = desmopressin
Nephrogenic Diabetes Insipidus
Causes;
- Genetic: the more common form affects the vasopression (ADH) receptor,
- electrolytes: hypercalcaemia, hypokalaemia
- drugs: demeclocycline, lithium
- tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis Treatment = thiazide diuretic
Side effects of EPO therapy
accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis
Indication for dialysis in acute renal failure (AEIOU)
A - severe acidosis E - Electrolytes I - Intoxicants O - Overload U - Uraemic symptoms
Secondary causes of hypokalaemia
- ) Increased potassium loss:
- Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics
- GI losses: diarrhoea, vomiting, ileostomy
- Renal causes: dialysis
- Endocrine disorders: hyperaldosteronism, Cushing’s syndrome - ) Trans-cellular shift
- Insulin/glucose therapy
- Salbutamol
- Theophylline
- Metabolic alkalosis
