Renal Medicine Flashcards
What features describe Stage 1 CKD?
eGFR > 90mL/min with evidence of renal damage e.g. proteinuria, haematuria
What features describe Stage 2 CKD?
eGFR = 60-89mL/min with evidence of renal damage e.g. proteinuria, haematuria
What features describe Stage 3A CKD?
eGFR = 45-59mL/min
What features describe Stage 3B CKD?
eGFR = 30-44mL/min
What features describe Stage 4 CKD?
eGFR = 15-29mL/min
What features describe Stage 5 CKD?
eGFR less than 15mL/min
What features describe Stage 1 AKI?
- Serum Creatinine increase >26umol/L in 48h
- OR increase creatinine 1.5 x baseline
- OR urine output less than 0.5mL/kg/hr for at least 6 consecutive hours
What features describe Stage 2 AKI?
- Serum Creatinine increase 2-2.9 x baseline
- urine output less than 0.5mL/kg/hr for at least 12hr
What features describe Stage 3 AKI?
- Serum Creatinine increase >3 x baseline
- OR creatinine over 354umol/L
- OR urine output less than 0.3mL/Kg/Hr for at least 24hr
- OR anuria for 12h
Describe IgA Nephropathy, its features, associated conditions, and prognosis.
IgA Nephropathy: also known as Berger’s disease or mesangioproliferative glomerulonephritis most common cause of glomerulonephritis worldwide due to IgA complex depositon.
Features: young male, recurrent episodes of macroscopic haematuria, concurrent infection Histology shows mesangial hypercellularity, positive immunoflourescene for IgA and C3.
Associated Conditions:
-Alcoholic cirrhosis, Coeliac disease, Henoch-schonlein purpura.
Prognosis:
- 25% develop ESRF
- Markers of good prognosis: Frank haematuria
- markers of poor prognosis: Male gender, proteinuria, hypertension, smoking, hyperlipidaemia, ACE genotype DD.
Describe Post-streptococcal glomerulonephritis, it’s symptoms,
Immune complex deposition that occurs 7-14days post strep infection most commonly in children.
Features: Headache, malaise, haematuria, nephritic syndrome, hypertension, low C3, raised ASO (AntiStreptolysin O) titre
Describe Alport’s syndrome and its features.
Alport’s syndrome is an inherited usually X-linked dominant disorder of type IV collagen resulting in abnormal glomerular basement membrane. Therefore more severe in males.
Features:
- Childhood presentation
- microscopic haematuria
- progressive renal failure
- bilateral sensorineual deafness
- retinitis pigmentosa.
- Lenticonus (protrusion of the lens surface into the anterior chamber)
- Renal biopsy may show splitting of the lamina densa on electron microscopy.
Alport’s patient with failing renal transplant think goodpasture’s like syndrome with presence of anti-GBM antibodies.
Define Nephrotic Syndrome, its causes, complications and management
Triad of Proteinuria >3.5g/24h (ACR >250mg/mmol), hypoalbuminaemia and oedema
Primary causes: Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis
Secondary causes: Hepatitis B/C, SLE, diabetic nephropathy, amyloidosis, paraneoplastic, drugs (NSAIDs, penicillamine, anti-TNF, gold)
Complications: susceptibility to infection, thromboembolism, hyperlipidaemia
Management:
- Reduce oedema (Loop diuretic),
- Reduce proteinuria (ACE-inhibitor, Angiotensin-Receptor Blocker)
- Reduce risk of complications (anticoagulate, statin), and Treat underlying cause.
Describe Minimal Change Disease and its treatment.
Commonest cause of nephrotic syndrome in children, biopsy normal under light microscopy. T-cell and cytokine mediated damaged to glomerular basement membrane leads to polyanion loss and the resultant reduction of electrostatic charge increased glomerular permeability to serum albumin.
Treatment:
- Spontaneous remission is possible, and remission can be induced with steroid therapy but may relapse (steroid-dependent) or be resistant (Steroid Resistant).
- Steroid-resistant disease or steroid-dependent disease can be treated with cyclophosphamide or tacrolimus. 1% progress to ESRF
Describe membranous nephropathy, its causes, Features, and management
Second most common cause of nephrotic syndrome in adults accounting for 20-30%.
Causes:
- Primary (Idiopathic) associated with M type phospholipase A2 and Neutral endopeptidase autoantibodies
- Infections: hepatitis B, Malaria, Syphilis
- Malignancy: Lung cancer, Lymphoma, Leukaemia
- drugs (NSAIDs, Gold, Penicillamine)
- Autoimmune (SLE, Thyroid, Rheumatoid)
Features:
- Nephrotic Syndrome
- Hypertension
- Biopsy shows diffusely thickened GBM with subepithelial deposits of IgG and C3 on immunofluorence. This creates a ‘Spike and dome’ appearance
Managment:
- Treatment involves managing nephrotic syndrome.
- Immunesuppression: A combination of corticosteroids +another agent such as chlorambucil is often used.
- Blood Pressure control: ACE inhibitors have been shown to reduce proteinuria.
- consider anticoagulation
- A third spontaneously remit, a third remain proteinuric, a third develop ESRF.
Describe mesangiocapillary glomerulonephritis, its features, types, and management.
Aka Membranoproliferative glomerulonephritis. May be immune complex mediated or complement mediated and may be due to underlying cause such as Hepatitis C, SLE, monoclonal gammaglobulinopathies.
Features:
- may present as nephrotic syndrome, haematuria, proteinuria
- Biopsy shows mesangial and endocapillary proliferation, thickened GBM and double contouring (tramline) of the capillary walls.
Types:
- Type 1, accounts for 90%, subendothelial immune deposits of electron dense material result in ‘tram-track’ appearance, Causes include cyroglobulinaemia, Hepatitis C.
- Type 2 aka dense deposit disease, there is reduced serum complement and C3b nephritic factor found in 70%, causes include partial lipodystrophy, factor H deficiency
- Type 3 caused by Hepatitis B+C
Management:
-Treat underlying cause and nephrotic syndrome.
prognosis poor when no underlying cause is found and in patients with ESRF if can reoccur in transplants.
-steroids may be effective
Describe focal segmental glomerulosclerosis (FSGS), its causes, features, and management
Most common cause of nephrotic syndrome in adults.
Causes:
May be primary (idiopathic) or secondary (Vesicoureteric reflux, IgA nephropathy, vasculitis, Alport’s syndrome, sickle-cell disease, heroin use).
Features:
Biopsy shows segmental glomerular scarring and IgM and C3 deposits on immunofluorence.
Management:
10% remit spontaneously, may respond to corticosteroids or cyclophosphamide if resistant. Can progress to ESRF and reoccur ~20% of transplants.
Describe Rhabdomyolysis, its causes and clinical features, and management.
Rapid muscle breakdown with release of K+, Phosphate, myoglobin, urate, and creatine kinase. This leads to hyperkalaemia and AKI due to renal tubule obstruction by myoglobin.
Causes include trauma (burns, crush injury, uncontrolled seizures), Drugs and toxins (statins, alcohol, ectasy, heroin, neuroleptic malingant syndrome), metabolic (hypokalaemia, myositis) and inheritied muscle disorders (duschenne’s muscular dystrophy, McArdle’s disease)
Clinical features: red-brown urine (visible myoglobinuria), muscle pain, hyperkalaemia, Increased phosphate, plasma CK >1000iU/L, hypocalcaemia, hyperuricaemia.
Management:
- Mostly supportive with rehydration aiming UO of 200-300ml/Hr
- Diuretics may be needed in those with risk of CCF and
- Urine alkalinastion may be use but evidence is poor
- haemodialysis may be neccesary if a candidate and continued poor renal function.
Name some nephrotoxic drugs
NSAIDs Antimicrobials e.g. gentamicin, sulfonamides, penicillins, rifampicin, amphotericin, aciclovir Anticonvulsants e.g. Lamotrigine, valproate, phenytoin Omeprazole furosemide, thiazides ace-inhibitors, ARBs cimetidine lithium, iron, cisplatin radiocontrast.
Describe Haemolytic Uraemic Syndrome (HUS)
Endothelial damage commonly (90%) from E.coli strain O157 leads to thrombosis, platelet consumption and fibrin strand deposition mainly in renal microvasculature. Strands cause mechanical destruction of RBC’s giving triad of haemolysis, thrombocytopenia and AKI. It is most common cause of AKI in children. Clinical features include abdominal pain, bloody diarrhoea and AKI.
Describe CKD, its causes, and management.
Impaired renal function for more than 3 months based on abnormal structure or persitantly reduced GFR
Causes:Diabetes (20%), hypertension or renovascular disease, glomerulonephritis (commonly IgA nephropathy also SLE, Vasculitis), Unknown, reflux nephropathy, or inherited disorders e.g. ADPKD, alports, Fabrys.
Management:
- Treat reversible causes
- BP less than 130/80 or 125/75 if diabetic or ACR>70
- Renal bone disease, check PTH and treat if raised, Phosphate rises in CKD, restrict dilate and consider binders, and calcium supplementation
- reduced CVS risk with statins
- dietician input, e.g. Moderate protein diet, potassium restriction, avoidance of high phosphate foods eg. Milk, cheese, eggs.
- symptom control for anaemia, acidosis, oedema, restless leg/cramps
- preparation for renal replacement in end stage CKD.
Describe Acute Tubular Necrosis (ATN)
Most common cause of AKI, characterised by death of tbular epithelial cells due to ischaemia most commonly caused by hypotension or nephrotoxic drugs.
The presence of “muddy brown casts” of epithelial cells found in the urine during urinalysis is pathognomonic for ATN
Describe Thrombotic Thrombocytopenic Purpura (TTP), its features, causes, and management.
Overlap with HUS, Due to an genetic or acquired deficiency of protease ADAMTS13 which normally cleaves VonWillebrand multimers. Large vWF Multimers form which cause platelet aggregation and fibrin deposition in small vessels, leading to microthrombi. Increased risk with clopidogrel
Features: Thrombocytopaenia, Microangiopathic haemolytic anaemia, Other features include AKI (nephritic), CNS involvement, fever.
Causes: Idiopathic (40%), autoimmune e.g. SLE, paraneoplastic, pregnancy, drugs (quinine),
Management:
- Do not infuse platelets
- plasma exchange
Describe transplant rejection
Can be acute or chronic. Acute is divided into humoral (anti-body mediated) or cellular (far commoner); usually treatment for either is high dose IV methylprednisolone and an intensification of immunosuppression. Antibody-mediated rejection often required plasma exchange in addition to clear donor-specific antibodies.
Chronic allograft nephropathy is thought to be a combination of chronic low-grade antibody response plus vascular changes and the effects of calcinuerin inhibitors or CNIs (tacrolimus). Generally does not respond to treatment but sometimes progression can be slowed by switching CNIs
Describe renal biopsy, its indication, pre procedure checks, contraindications and complications
Patients lay on their front, local anaethetic used and core biopsy taken. Bed rest on back for minimum of 6h
Indications:
- unexplained AKI or CKD
- acute nephritic syndrome
- unexplained proteinuria or haematuria
- suspected transplant rejection
- systemic disease associated with kidney dysfunction
Pre procedure check: FBC, clotting, group and save. obtain written consent. Ultrasound to delineate anatomy (Horseshoe kidney?, two kidney? Size?). Stop anticoagulants (asprin 1 wk, wafarin 3 days, LMWH 1 day)
Contraindications:
- abnormal clotting
- hypertension greater than 160/90mmHg
- single kidney
- CKD with small kidneys (less than 9cm)
- uncooperative patient
- horseshoe kidney
- renal neoplasms.
Complications:
- Bleeding, macroscopic haematuria occurs in 1/10
- Bleeding requiring transfusion in 1/100
- nephrectomy rare
What are the indications of dialysis?
- hyperkalaemia unresponsive to medical treatment or in an oliguric patient
- Pulmonary oedema unresponsive to medical treatment
- uraemic complications such as pericarditis or encephalopathy
- severe metabolic acidosis unresponsive to treatment (pH less than 7.1)
- drug toxicity
Describe Renal tubular acidosis, its types, and treatment.
Is a metabolic acidosis due to impaired acid secretion by the kidney. There is a hyperchloraemic metabolic acidosis with normal anion gap.
Types: There are 4 types and type 3 is a combination of type 1 and 2.
- Type 1 (distal) RTA is due to a failure of alpha-intercalated cells in the collecting tubules to secrete H+ and reclaim K+
- Type 2 (proximal) is due to a ‘bicarbonate leak’ a defect in HCO3 reabsorption in the proximal tubule resulting in excess HCO3 in the urine and hypokalaemia.
- Type 4 (hyperkalaemic) is due to hyporeninaemic hypoaldosteronism. hypoaldosteronism causes hyperkalaemia and acidosis.
Treatment: is with bicarbonate.
Describe nephritic syndrome and its causes.
Nephritic syndrome includes haematuria, proteinuria, hypertension and ureamia.
Primary causes include IgA nephropathy and mesangiocapillary glomerulonephritis.
Secondary causes include post-streptococcal, vasculitis, SLE, Goodpastures, cryoglobulinaemia.
Describe Hyperkalaemia, its signs, symptoms, causes and treatment
Plasma potassium >6.5mmol/L, increased potassium leads to myocardial hyperexcitability leading to ventricular fibrillation and cardiac arrest.
Signs + symptoms: Fast irregular pulse, chest pain, weakness, palpitations, light-headedness. ECG shows tall tented T waves, possibly VF.
Causes: oliguric renal failure, K sparing diuretics e.g. spironolactone, Rhabdomyolysis, Metabolic Acidosis (DM), Excess K therapy (iatrogenic), Addison’s disease, Massive blood transfusion, Burns, Drug causes e.g. ACE-i, Artefactual result.
Treatment:
- stabilise cardiac membrane with 10mL of 10% calcium gluconate over 10mins.
- drive K+ into cells with 10units of insulin and 500ml 10% dextrose over 60mins
- using non-potassium sparing diuretics such as furosemide and also calcium resonium with lactulose to increase K excretion
- resistant hyperkalaemia despite treatment is an indication for dialysis
Describe Syndrome of Inappropriate ADH secretion (SIADH), it’s causes, and management.
A cause of hyponatraemia and decreased Urine output, SIADH consists of:
-concentrated urine (Na+ > 20mmol/L, osmalility >100mosmol/kg)
-hyponatraemia (plasma Na less than 125mmol/mL)
-low plasma osmolality (less than 260mosmol/kg)
in the absence of hypovolaemia, oedema or diuretics
Causes:
- malignancy e.g. Lung small cell, pancreas, prostate, thymus, lymphoma
- CNS disorders e.g. Menigoencephalitis, abscess, stroke, subarachnoid or subdural haemorrhage, head injury, neurosurgery, guillain-barre, SLE, Vasculitis
- Chest disease e.g. TB, pneumonia, abscess, aspergillosis, small cell lung cancer
- Endocrine e.g. Hypothyroidism
- Drugs e.g. Sulfonylureas, SSRIs, tricyclics, carbamazepine, vincristine, cyclophosphamide.
- Other e.g. Acute intermittent porphyria, trauma, abdominal or thoracic surgery, symptomatic HIV.
Management:
- identify and treat the cause
- Slow correction to avoid pontine myelinolysis
- fluid restriction
- domeclocycline reduces responsiveness of collecting tubule cells to ADH
- ADH antagonist may have a role.
What are the causes of Hyperuricaemia?
Drugs: Cytotoxics, Thiazides, Loop Diurectics, pyrazinamide
Increased Cell Turnover : lymphoma, leukaemia, psoriasis, haemolysis, rhabdomyolysis, tumour lysis syndrome
Reduced Excretion: primary gout, chronic kidney disease, lead nephropathy, hyperparathyroidism, pre-eclampsia
Describe Acute Urinary Retention, its causes, symptoms, and management
Causes: prostatic obstruction (usual cause in males), urethral strictures, anticholinergics, alcohol, constipation, post-op, infection, neurological (cauda equina syndrome), carcinoma.
Symptoms: Tender bladder, anuria, dull percussion of bladder.
Management:
- MSU, U+E, FBC, and PSA to help identify cause.
- Conservative management: tricks to aid voiding such as analgesia, privacy on hospital wards, ambulation, standing to void, voiding to sound of running taps or in a hot bath.
- Other wise Catheterise and start an alpha-blocker e.g. Tamulosin.
- Monitor for post-obstructive diuresis, in acute phase after relief of the obstruction, the kidneys produce a lot of urine, match input to output.
- TWOC
Describe Hypokalaemia, it’s signs and symptoms, causes, and management
If K+ less than 2.5mmol/L, urgent treatment is required. Note that Hypokalaemia exacerbates digoxin toxicity. Mg2+ may be low and Hypokalaemia is difficult to correct until these levels are restored. GISSI-2 Trial observed that serum K less tan 3.6mmol/L was associated with a twofold increase in VF + Non-sustained VT.
Signs and Symptoms: Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness (arrhytmias), constipation
Causes: Diuretics (Increased HCO3 supports this), D+V, pyloric stenosis, rectal villous adenoma, intestinal fistula, Cushing’s syndrome/steroids/ACTH, Conn’s syndrome, alkalosis, renal tubular failure.
Management:
- oral K+ supplement if greater than 2.5 and asymptomatic
- If taking thiazide diuretic and K+ greater than 3 consider repeating and/or changing to K+ sparing e.g. Spironolactone
- If severe i.e. Less than 2.5mmol/L or symptomatic, give IV potassium cautiously, not more than 20mmol/hr and not more concentrated than 40mmol/L. Do not give K+ if oliguric and never give as a stat bolus dose.
