Renal Medicine Flashcards
(83 cards)
1
Q
What features describe Stage 1 CKD?
A
eGFR > 90mL/min with evidence of renal damage e.g. proteinuria, haematuria
2
Q
What features describe Stage 2 CKD?
A
eGFR = 60-89mL/min with evidence of renal damage e.g. proteinuria, haematuria
3
Q
What features describe Stage 3A CKD?
A
eGFR = 45-59mL/min
4
Q
What features describe Stage 3B CKD?
A
eGFR = 30-44mL/min
5
Q
What features describe Stage 4 CKD?
A
eGFR = 15-29mL/min
6
Q
What features describe Stage 5 CKD?
A
eGFR less than 15mL/min
7
Q
What features describe Stage 1 AKI?
A
- 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
8
Q
What features describe Stage 2 AKI?
A
- Serum Creatinine increase 2-2.9 x baseline
- urine output less than 0.5mL/kg/hr for at least 12hr
9
Q
What features describe Stage 3 AKI?
A
- 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
10
Q
Describe IgA Nephropathy, its features, associated conditions, and prognosis.
A
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.
11
Q
Describe Post-streptococcal glomerulonephritis, it’s symptoms,
A
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
12
Q
Describe Alport’s syndrome and its features.
A
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.
13
Q
Define Nephrotic Syndrome, its causes, complications and management
A
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.
14
Q
Describe Minimal Change Disease and its treatment.
A
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
15
Q
Describe membranous nephropathy, its causes, Features, and management
A
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.
16
Q
Describe mesangiocapillary glomerulonephritis, its features, types, and management.
A
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
17
Q
Describe focal segmental glomerulosclerosis (FSGS), its causes, features, and management
A
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.
18
Q
Describe Rhabdomyolysis, its causes and clinical features, and management.
A
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.
19
Q
Name some nephrotoxic drugs
A
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.
20
Q
Describe Haemolytic Uraemic Syndrome (HUS)
A
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.
21
Q
Describe CKD, its causes, and management.
A
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.
22
Q
Describe Acute Tubular Necrosis (ATN)
A
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
23
Q
Describe Thrombotic Thrombocytopenic Purpura (TTP), its features, causes, and management.
A
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
24
Q
Describe transplant rejection
A
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
25
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
26
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
27
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.
28
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.
29
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
30
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.
31
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
32
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
33
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.
34
Describe Urinary Tract Calculi (aka kidney stones, nephrolithiasis), it's presentation, investigations and management.
Renal stones consist of crystal aggregates. Stones form in collecting ducts and may be deposited anywhere from the renal pelvis to the urethra.
Signs and symptoms: Asymptomatic, Renal colic (severe waxing and waning loin pain radiating to the groin or thigh, with fever or vomiting), Renal obstruction (loin pain), obstruction of mid-ureter may mimic appendicitis/diverticulitis. UTI can co-exist (burning sensation, increased urinary frequency), as can pyelonephritis (fevers, rigours, loin pain, nausea and vomiting).
Investigations:
- Bloods: FBC, U+E, Ca2+, PO43-, glucose, bicarbonate, urate.
- Urinalysis usually +ve for blood (90%)
- MSU: MC+S
- Imaging, KUB (80% identified), or spiral non-contrast CT is best.
Management:
- Analgesia e.g. Diclofenac 75mg IV/IM or 100mg PR, if CI opioids.
- Antibiotics e,g, Cefuroxime 1.5mg/8h IV if infection
- Stones less than 5mm pass spontaneously, increase fluid intake
- stones greater than 5mm or pain not resolving require medical expulsion therapy with nifedipine 10mg/8h or tamsulosin 0.4mg/
- if fails try extracorporeal shockwave lithotripsy (SEs renal injury, may also cause hypertension and DM)
- If larger than 2cm or staghorn consider percutaneous nephrolithotomy
- infection and ureteric obstruction is a surgical emergency and requires decompression with nephrostomy tube placement or insertion of ureteric stents.
35
Describe Polycystic Kidney disease, symptoms, and management.
Autosomal dominant, 85% have a mutation in PKD1 on chromosome 16 and 15% in PKD2 in chromosome 4. The first type present with renal failure earlier.
Symptoms: Renal enlargement with cysts causing abdominal pain +/- haematuria, and hypertension. May also have extrarenal symptoms such as liver cysts, SAH, mitral valve prolapse, ovarian cysts, diverticular disease.
Management:
-monitor U+E, increase water intake, reduce Na and caffeine intake.
-BP treated aggressive targeting less than 130/80 ACE-I are best choices.
-dialysis + transplantation for ESRF.
-
36
Describe Bartter's syndrome and its symptoms.
An autosomal recessive cause of severe Hypokalaemia due to defective chloride absorption at the NKCC2 in the ascending loop of Henle. It is Socrates with normotension unlike other causes of Hypokalaemia such as Conn's, Cushings and Liddles.
Symptoms: Polyhydraminos in utero, Failure to thrive, Polyuria, polydipsia, Hypokalaemia, normotension, weakness. Increased Urinary Calcium
37
Describe Hyponatraemia, its symptoms, causes, investigations and management.
Mild Hyponatraemia (Na 130 -135), Moderate (Na 120-130), Profound (Na less than 120). Severe hyponatratemia is reserved for those with signs of raised ICP. May be split depending on plasma Osmolality and patients fluid status.
Symptoms: mostly asymptomatic but risk of cerebral oedema so look for signs of raised ICP e.g. vomiting, drowsiness, headache, pappiloedema, and late signs such as coma, seizures, bradycardia, hypertension, opthalmoplegia
Cause: If plasma osmolality is normal ?pseudo-Hyponatraemia (artefact due to raised lipid/protein) or high (consider hyperglyaceamia)
Hypotonic may be split into:
-hypovolaemic: GI loss, Burns, renal loss (thiazides), addisons, third space losses (GI obstruction, pancreatitis, sepsis) salt-wasting nephropathies (post-chemo tubulopathy), diabetes inspidus
-euvolaemic: SIADH, secondary adrenal insufficiency, hypothyroidism, primary polydispsia, anorexia nervosa, beer potomania
-Hypervolaemic: Heart failure, Liver failure, CKD, nephrotic syndrome
Investigations: Repeat sodium, plasma and urine osmalility, fluid status?, U+E (?renal disease), TFT (?hypothyroidism), Morning serum cortisol (?addisons), LFT (?liver disease), BNP(?Heart failure), serum and urine electrophoresis(myeloma) FBC (?malignancy), CXR (? Lung cancer).
Management:
- get help and avoid quick restoration (less than 10mmol/L/day) of Hyponatraemia due to risk of osmotic demyelination syndrome (can occur upto 5 days after, paralysis is main symptom)
- if hypovoleamic resuscitate cautiously with 0.9% saline
- if symptomatic 2.7% hypertonic saline over 30mins
- otherwise fluid restriction and treat underlying cause
38
Describe AKI, its risk factors, causes, complications, and management
Rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine, leading to a failure to maintain fluid, electrolyte and acid-base homeostasis.
Risk factors: 75yrs+, CKD, diabetes, cardiac failure, PVD, chronic liver disease, drugs, sepsis, hypovolaemia, Hx of urinary symptoms
Causes:
- Pre-Renal (40-70%) due to renal hypoperfusion e.g. Hypovolaemia, sepsis, renal artery stenosis + ACE-i.
- Intrinsic (10-50%) may require renal biopsy, acute tubular necrosis is most common intrinsic as a result of pre renal damage or nephrotoxins, rhabdomyolysis, radiocontrast, myeloma, hypercalacaemia. Glomerular causes e.g. Autoimmune such as SLE, HSP, glomerulonephritis. Vasculitis, tumour lysis syndrome, hypertension.
- Post-renal (10-25%) cause by urinary tract obstruction e.g. Stones, clots, malignancy, strictures.
Complications: Hyperkalaemia, Hyperuraemia, Pulmonary Oedema, Metabolic acidosis
Management:
- assess fluid status and aim for euvolaemia
- stop nephrotoxic drugs
- dip urine, look for cause
- catheterise monitor output
- manage compilations and consider haemodialysis if acidaemia less than 7.2, persistent hyperkaelamia over 7mmol/L, refractory pulmonary oedema, or uraemia complications such as encephalopathy or pericarditis
39
Describe Hypercalcaemia, its causes, symptoms, and management.
Causes: Primary hyperparathyroidism, malignancy, thiazide diuretics, sarcoidosis, thyrotoxicosis, vitamin D intoxication, lithium, familial hypocalciuric hypercalcaemia
Symptoms: "stones, bones, groans, psychic moans", abdominal pain, vomiting, constipation, polyuria, polydipsia, depression, anorexia, weight loss, fatigue, weakness, hypertension, confusion, renal stones, renal failure, decreased QT interval.
Management:
- Investigate cause, FBC, protein electrophoresis, PTH, vit D, 24hr urinary excretion, CXR, dexa scan.
- IV fluids to bring calcium down, dexamethasone if malignancy related.
- Severe hypercalcaemia (over 3.5mmol/L) administration of Calcitonin (4IU/Kg) and repeat Ca measurement in several hours. Also concurrent administration of Zoledronic acid (4mg IV over 15minutes) or pamidronate (60-90mg over two hours)
- Denosumab (60mg SC initially with repeat dosing based upon response) is also an option in refractory cases
40
Describe Hypocalcaemia, its causes, symptoms, and management
Causes: Primary hypoparathyroidism, renal failure, vitamin D deficiency, malabsorption, hypomagnesaemia
Symptoms: 'SPASMODIC" Spasms (Carpopedal, trousseau sign), Perioral paraesthesia, Anxious, Seizures, Muscle tone increased in smooth muscle (colic, wheeze, dysphagia), Orientation impaired, Dermatitis, Impetigo herpetiformis, Chvosteks sign (corner of mouth twitches when facial nerve tapped), cataract, cardiomyopathy (long QT on ECG)
Management:
- if mild give calichew 3g orally
- may need activated vitamin D - alfacalcidol especially in CKD
- If severe give IV 10ml 10% calcium gluconate over 30mins
41
Describe Renal Osteodystrophy and its management
Renal osteodystrophy is a form of metabolic bone disease that occurs in chronic kidney disease as result of hyperparathyroidism secondary to hyperphosphatemia and hypocalcaemia due to decreased excretion of phosphate by the damaged kidney. This is exacerbated as the kidney damage reduces the ability to convert Vitamin D3 into its active form causing further hypocalcaemia and a secondary hyperparathyroidism. After prolonged stimulation to produce PTH this can turn into tertiary hyperparathyroidism in which glands act autonomously having undergone hyperplastic changes and release excessive PTH pushing calcium above normal levels, occurs in chronic renal failure Phosphate will still be high differentiating it from other causes of hypercalcaemia.
Management:
- Calcium and Calcitriol (Active Vitamin D3)
- Restriction of dietary phosphate
- Phosphate binders such as calcium carbonate
- Renal transplant / Parathyroidectomy for symptomatic medication refractive end stage disease
42
Describe Rapidly Progressive Glomerulonephritis, its features, and management
The most aggressive GN, with potential to cause ESRF over days. There are different causes all have the histilogical finding of crescentic lesions affecting most glomeruli. Its classified into 3 groups:
- immune complex disease (45%) e.g. Post-infectious, SLE, IgA/HSP
- Pauci-immune disease (50%, 80-90% ANCA +ve) e.g. Granulomatosis with polyangiitis (Wegner's c-ANCE +ve), Chung-Strauss syndrome, microscopic polyangitis (p-ANCA+ve)
- Anti-GBM disease (3%) - goodpasture disease.
Features: AKI +/- systemic features e.g. Fever, malaise, weight loss, haemoptysis (pulmonary haemorrhage is the commonest cause of death in ANCA+ve patients).
Management:
-aggressive immunosupression with high dose IV steroids and cyclophosphamide +/-plasma exchange
43
Describe Acute interstitial Nepritis (AIN) its causes, features, and management.
Mediated by an immune reaction to drugs, infection of autoimmune disorders.
Causes:
- Drugs: NSAIDs, antibiotics, diuretics, allopurinol, omeprazole, phenytoin
- Infections: Staph, strep, brucellosis, leptospirosis
- Immune disorders: SLE sarcoid, idiopathic
Features: usually mild Renal impairment. Drug causes may give allergic picture with fever rash and peripheral eosinophilia. Biopsy shows inflammatory cell infiltrate in the interstitium.
Management:
- stop causative agent
- if renal function doesn't improve trial prednisolone 1mg/kg/24h for 4wks
44
Describe Chronic Interstitial Nephritis (CIN)
Common in disorders leading to abnormal anatomy e.g. Reflux nephropathy, cystic kidney disease. Can also be induced by drug causes, and autoimmune disorders and haematological disorders.
45
What is the rule of 3's regarding ACR?
Normal ACR less than 3mg/mmol (less than 30mg/g -Grade A1 Albuminuria
3-30mg/mmol (30-300mg/g) moderately increased - Grade A2 Albuminuria
Over 30mg/mmol (Over 300mg/g) severely increased - Grade A3 albuminuria
46
What are the different types of renal stones?
Calcium Oxalate 85%, hypercalcaeia is a risk factor, stones are radio-opaque.
Cystine 1% inherited recessive disorder of transmembrane cysteine transport leads formation of these stones in younger patients radio-opaque
Urate 5-10%, may precipitate when Urinary pH is low, occur in disease with extensive tissue breakdown e.g. Malignancy, rhabdo; more common in children with inborn errors or metabolism, they are radio-lucent
Calcium phosphate 10%, occur in renal tubular acidosis type 1 + 3, high urinary pH increases formation. Radio-opaque
Struvite 2-20% Staghorn calculi, occur as a result of urease producing bacteria. Radio-opaque. Also more likely in alkaline urine.
47
What is orthostatic proteinuria?
Increased daytime protein excretion associated with activity and upright posture. Positive protein on urine dipstick during day but negative tests with early morning urine. All other investigations of renal function are normal. 24hr Protein collection usually normal/ less than 1g per 24hrs.
48
Describe Fibromuscular dysplasia, its features and management.
An autosomal dominant disorder mostly affecting females aged 15-50years. Characterised by arterial stenosis predominantly in the renal arteries, carotid arteries and less commonly the mesenteric arteries. Stenosis occurs due to abnormal proliferation of vascular endothelial cells and results in the classical 'string of beads' appearance on angiography.
Features: Hypertension, Renal impairment, Mesenteric ischaemia, TIA
Management
-Angioplasty
49
Describe Gitelman's syndrome and its features
Autosomal recessive condition associated with reduced Na + Cl reabsorption due to defect in Na/Cl transporter in the distal convoluted tubule (site of action of Thiazides)
Features: Hyponatraemia, Hypochloraemia, high urinary sodium, low urinary calcium. Hypokalaemic metabolic alkalosis (due to increased aldosterone secretion).
50
Describe Liddle's syndrome and its features.
Rare autosomal dominant condition associated with mutations in the epithelial sodium channels.
Features: Hypertension, low aldosterone levels, hypokaelaemic metabolic alkalosis
51
Describe Peritoneal Dialysis, its and complications.
A form of renal replacement therapy. It is sometimes used as a stop-gap to haemodialysis or for younger patients who do not want to have to visit hospital three times a week.
The majority of patients do Continuous Ambulatory Peritoneal Dialysis which involves four 2 litre exchanges/Day
Complications: Peritonitis coagulase-negative staphylococci such as Staph Epidermidis are most common. Staph Aureus is another common cause.
Sclerosing peritonitis.
52
Describe the management of Anaemia in CKD
Consider management when Hb is less than 11g/dL and aim to maintain between 10-12g/dL.
Treatment is with Eythropoetin, its is contraindicated in uncontrolled hypertension and potential side effects include, worsening hypertension, headache, increased platelets, Flu-like symptoms, hyperkalaemia, and skin reactions.
Other factors which contribute to anaemia should be corrected before treatment e.g. Iron of folate deficiency.
53
Describe Renal Vein Thrombosis, its features and management.
Usually occurs in newly born infants with blood clotting abnormalities or dehydration and adults with nephrotic syndrome.
Symptoms: Sudden onset flank pain, sudden decrease in renal function, PE, haematuria.
Investigations: CT Angiography
Management:
- Anticoagulation
- Treat cause
54
Describe type 1 Renal tubular acidosis, its features, causes, and complications.
Inability to generate acid urine (secrete H+) in distal tubule.
Features:
-hypokalaemia and hyperchloraemia metabolic acidosis (normal anion gap), Low urinary citrate, Hypercalcuria, Urine pH greater than 5.3
Causes: Idiopathic, RA, SLE, Sjrogens, amphotericin B toxicity, analgesic nephropathy.
Complications include nephrocalcinosis and renal stones
55
Describe Type 2 Renal Tubular Acidosis
Deceased HCO3- reabsorption in proximal tubule Cause hypokalaemia
Complications include osteomalacia
Causes include idiopathic, as part of Fanconi Syndrome, Wilson's disease, cystinosis, Outdated tetracyclines, multiple myeloma
56
Describe Type 4 Renal Tubular Acidosis
Reduction in aldosterone leads in turn to a reduction in proximal Tubular ammonium excretion
Causes hyperkalaemia
Caused include hypoaldosteronism, diabetes.
57
Describe Renal Papillary Necrosis, its features, and causes.
Renal papillary necrosis describes the coagulative necrosis of the renal papillae due to a variety of causes.
Features:
- Frank Haematuria
- Loin pain
- Proteinuria
Causes (POSTCARDS):
- Pyelonephritis
- Obstruction
- Sickle Cell Disease
- Tuberculosis
- Cirrhosis
- Analgesic abuse
- Renal Vein Thrombosis
- Diabetes
- Systemic Vaculitidies
58
What are the cut offs for a normal and abnormal urine output?
```
Normal = 1ml/kg/hr
Abnormal = less than 0.5ml/kg/hr
```
59
Describe Fanconi syndromem its features,and its causes.
Fanconi syndrome describes a generalised disorder of renal tubular transport in the proximal convoluted tubule
Features:
- type 2 (proximal) renal tubular acidosis
- polyuria
- aminoaciduria
- glycosuria
- phosphaturia
- osteomalacia
Causes:
- Cystinosis (most common cause in children)
- Sjrogren’s syndrome
- multiple myeloma
- Nephrotic syndrome
- Wilson’s disease
60
Describe some features that can differentiate Pre-renal uraemia and acute tubular necrosis.
Urine sodium: Less than 20mmol in pre-renal, over 30 in ATN
Fractional sodium excretion: Less than 1% in Pre-renal, Over 1% in ATN
Fractional Urea excretion: Less than 35% in Pre-renal, Over 35% in ATN
Urine:Plasma Osmalility: greater than 10:1 in pre-renal, less than 8:1 in ATN
Specific gravity: Over 1020 in pre-renal, less than 1010 in ATN
Urine: Bland sediment in pre-renal, Brown granular casts in ATN
Response to fluid challenge: Good response in Pre-renal, poor response in ATN.
61
Describe the stages of diabetic nephropathy.
Stage 1: Hyperfiltration (increase in GFR) may be reversible.
Stage 2 (Silent or latent phase): Most Patients do not develop microalbuminaemia for 10years GFR remains elevated
Stage 3 (Incipient nephropathy): Microalbuminuria (albumin excretion of 30-300 mg/day, dipstick negative).
Stage 4 (Overt nephropathy): Persistent proteinuria (Albumin excretion over 300mg/day, dipstick positive), Hypertension is present in most patients, histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson Nodules)
Stage 5: End-stage renal disease, GFR <10ml/min, renal replacement therapy needed.
62
Describe the Urine Osmolal Gap and its use.
A method to qualitatively estimate the urine NH4 concentration. Under most condition, the urine osmalility is generated by sodium salts, potassium salts, urea, glucose, and ammonium salts. Thus if the urine osmolality is actually measured and calculated using the measured concentrations of the respective ions the difference should represent the concentration of ammonium salts.
Formula: Measured urine osmolality - ((2 x (Urine Na + Urine K) + Urine Urea + Urine Glucose)
The major renal response to chronic metabolic acidosis is increased NH4 excretion. If this value is not increased it suggests impairment in ammonium excretion thus:
A UOG less than 150mosmol/kg in a patient with chronic metabolic acidosis suggest that NH4 excretion is impaired. Because ammonium excretion is reduced in patients with distal renal tubular acidosis, a low UOG is consistent with diagnosis. It is also consistent with type 4 RTA.
A UOG exceeding 400mosmol/kg is likely that urine NH4 concentration is also higher. this would be expected with hypercholeremic metabolic acidosis that is generated by chronic diarrhoea, by inhalation of toluene, and by other disorders in which then renal response to academia remains intact.
63
Describe Metabolic Acidosis, its assessment and its causes.
Metabolic acidosis can be produced by three major mechanisms:
- Increased Acid generation e.g. lactic acidosis, ketoacidosis, salicylate poisoning, Methanol, ethylene glycol.
- Loss of bicarbonate e.g. severe diarrhoea, Proximal Type 2 renal tubular acidosis
- Diminished Renal Acid excretion e.g. reduced GFR, distal Type 1 RTA and type 4 RTA.
Causes can be further differentiated by Anion Gap.
64
Describe Cholesterol Embolisation and its features
Cholesterol emboli in hypercholesterolaemic patients may break off causing renal disease. Seen more commonly in ateriopaths, abdominal aortic aneurysms.
Features:
- Eosinophilia
- Purpura
- Renal Failure
- Livedo Reticularis
65
What are the different causes of Glomerulonephritis according to associated complement levels?
Low Complement GN:
- Systemic: SLE, endocarditis, Cyroglobulinaemia
- Isolated Renal: Post-Streptococcal GN, MPGN
Normal Complement GN:
- Systemic: HSP, ANCA associated (GPA, PAN), Goodpasture's, Hypersensitivity vasculitis
- Isolated Renal: IgA Nephropathy, Anti-GBM disease, RPGN
66
Describe Autosomal Recessive Polycystic Kidney Disease and its features.
Much less common than Autosomal Dominant PKD. It is due to a defect in a gene located on chromosome 6 which encodes fibrocystic, a protein important for normal renal tubule development.
Diagnosis may be made on prenatal ultrasound or in early infancy with abdominal masses and renal failure. Newborns may also have features consistent with Potter's syndrome secondary to oligohydraminos. End stage renal failure develops in childhood. Patients also typically have liver involvement, for example portal and interlobular fibrosis.
Renal Biopsy typically shows multiple cylindrical lesions at right angles to the cortical surface.
67
Describe HIV-associated Nephropathy (HIVAN) and its features.
Renal involvement in HIV patients may occur as a consequence of treatment or the virus itself. Protease inhibitors such as indinavir can precipitate intratubular crystal obstruction.
HIV-associated Nephropathy (HIVAN) accounts for up to 10% of end-stage renal failure cases. Antiretroviral therapy has been shown to later the course of the disease. The 5 key features are:
- Massive proteinuria
- Normal or large kidneys
- Focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
- Elevated urea and creatinine
- Normotension
68
Describe Potter's Syndrome and its features
Describes the typical physical appearance caused by pressure in utero due to oligohydraminos, classically due to Bilateral Renal Agenesis, but can occur with other conditions.
Features:
- Ultrasound may show renal agenesis
- Hydronephrosis
- Hyperechoic foetal kidneys (suggestive of polycystic kidney disease)
- Flattened Parrot-beaked nose, recessed chin, prominent epicentral folds, low-set cartilage deficiency ears.
- pulmonary hypoplasia
- Cataract, angiomatous malformation in the optic disc, prolapse of lens
- VSD, endocardial cushion defect, Fallot's tetralogy, PDA.
- Clubbed feet, malformed hands, sacral agenesis, hemivertebrae, limb contractures
69
Describe Renal Artery Stenosis, its features, investigations, and management.
Narrowing of one of the renal arteries, most often causes by atherosclerosis or fibromuscular dysplasia. Reduced blood flow to kidney leads to renovascular hypertension, CKD.
Features: Asymptomatic, refractory hypertension, episodes of flash pulmonary oedema.
Investigations:
- Doppler ultrasound of kidneys
- Renal Bruit
- Captopril challenge test (measures change in renin plasma levels after administration of Captopril, large increase or high baseline is sensitive but not specific)
- Renal artery angiogram.
Management:
- Anti-hypertensives and diuretics
- minimally invasive angioplasty with or without stenting (best option if fibromuscular dysplasia).
70
Describe Cholesterol Embolisation and its features
Cholesterol emboli may break off causing renal disease, seen more commonly in arteriopaths, abdominal aortic aneurysms.
Features:
- Eosinophilia
- Purpura
- Renal failure
- Livedo Reticularis
71
Describe Kimmelstiel-Wilson syndrome
The mechanism by which proteinuria leads to glomerulosclerosis. Widening of the basement membrane usually by early diabetic nephropathy leads to an increase in the number of mesangial cells and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces periodic-acid schiff +Ve deposits called Kimmelstiel-Wilson Nodules. These nodules progessively expand and consume the entire glomerulus shutting off filtration
72
What are the different types of lupus nephritis?
Type I: Abnormal urine sediment with normal light microscopy, does not require immunosupression.
Type II: Mesangioproliferative glomerulonephritis
Type III: Focal glomerulonephritis. Requires immunosupression.
Type IV: Proliferative glomerulonephritis. Affecting over 50% of glomeruli often with crescents present. Frequently progresses to advanced CKD if untreated. Should be treated with immunosuppressant i.e prednisolone +/- Cyclophosphamide/mycophenolate.
Type V: membranous nephropathy.
Type VI: Advanced Sclerosed. Does not require immunosuppresion.
73
Describe Dialysis Related Amyloidosis
Characterised by accumulation and tissue deposition of amyloid fibrils consisting of beta2-microglobulin in the bone, periarticular structs, and viscera in patients on dialysis. Particularly present in those on dialysis for over 5 year.
74
Describe Dialysis Disequilibrium syndrome.
The occurrence of neurological signs and symptoms attributed to cerebral oedema during or shortly after intermittent haemodialysis. Classically arises in individuals starting haemodialysis in particular with 'aggressive' high solute removal dialysis.
75
What is the ideal diet in patients with CKD?
Low salt
Low Protein
Low Phosphate
76
What is the Ideal diet in patients on haemodialysis?
Low salt
High Protein
low phosphate
Fluid Restrict
77
Describe Xanthogranulomatous pyelonephritis, its features, and management.
A rare form of chronic pyelonephritis. Chronic infection leads to replacement of kidney with mass of reactive tissue usually surrounding a staghorn calculus with associated hydronephrosis. Foamy (Lipid-laden) macrophages predominate.
Features: Malaise, Weight loss, low grade pyrexia. Haematuria and flank pain may occur.
Management: Surgical nephrectomy.
78
Describe Medullary Sponge Kidney, its features, and management.
Aka Cacchi-Ricci Disease. A congenital disorder of the kidneys characterised by dilatation of the collecting tubules in one or bot kidneys.
Features: Reccurent UTIs, Recurrent Kidney Stones. Haematuria.
Can cause Distal Renal Tubular Acidosis (Type 1 RTA), CKD.
Management:
- U/S Kidney shows hyperechoic papillae wit clusters of small stones. (Paintbrush like appearance seen on HR Helcal CT.
- Adequate hydration
- Potassium citrate in those with hypocitraturia and incomplete distal renal tubular acidosis.
79
Describe erythropoietin and its role in treatment of anaemia.
A hormone produced by kidney to increased production of RBCs
Serum erythropoietin may be reduced in chronic renal failure and some cases of IDDM.
If serum EPO is less than 100, anaemia is likely to respond to EPO 100-500 should consider a trial but over 500 response is unlikely.
In secondary polycythaemia EPO is raised
In primary it is normal or reduced.
In anaemia treated with EPO target hB is 110. A Cochrane meta-analysis suggested that treating to a high target of 135 resulted in an increase risk of hypertensive crises.
Note rare side effect of EPO is EPO induces seizures occurs in first 90 days
80
What precautions are taken to reduce the risk of Contrast-induced Nephropathy?
Pre and post hydration with normal saline
Some evidence that NAC pre and post reduce the risk but no evidence to say it reduces mortality or risk of CIN needing Dialysis.
81
Which renal disease’s are associated with a high recurrence rate in transplanted kidneys?
```
Membranoproliferative Glomerulonephritis (30-90%)
Focal Segmental Glomerulosclerosis (40%)
Membranous Glomerulonephritis (30%)
```
82
Describe Nephrogenic systemic fibrosis, and its features
A cutaneous dermopathy seen in patients with end stage renal failure whom have been exposed to gadolinium containing contrast agents.
Features: pulmonary fibrosis, cardiomyopathy, pulmonary hypertension. Fibrotic skin
83
Describe Calciphylaxis, its features.
A life threatening condition most often seen in late stage chronic kidney disease on dialysis. Calcium deposits in the cutaneous arteries leading to Thrombosis and ischaemic necrosis, with refractory ulcers often in the lower extremities, abdomen or buttocks.
Features: Livedo Reticuloaris, Thrombosis, infraction black leathery Escher in an ulcer with adherent black slough.
