Renal Medicine Flashcards
A 17-year-old man is referred to the local nephrology unit for investigation. He reports having several episodes of visible haematuria. There is no history of abdominal or loin pain. These typically seem to occur within a day or two of developing an upper respiratory tract infection. Urine dipstick is normal. Blood tests show the following:
Na+141 mmol/l
K+4.3 mmol/l
Bicarbonate25 mmol/l
Urea4.1 mmol/l
Creatinine72 µmol/l
What is the most likely diagnosis?
Chlamydia
Bladder cancer
IgA nephropathy
Rhinovirus-associated nephropathy
Post-streptococcal glomerulonephritis
IgA nephropathy (also known as Berger’s disease) is the commonest cause of glomerulonephritis worldwide. It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.
- *Associated conditions**
- Alcoholic cirrhosis
- Coeliac disease/dermatitis herpetiformis
- HSP
Pathophysiology
mesangial deposition of IgA immune complexes - considerable pathological overlap with Henoch-Schonlein purpura (HSP).
Investigations:
Histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3
Presentations
- young male, recurrent episodes of macroscopic haematuria
- typically associated with a recent respiratory tract infection
- nephrotic range proteinuria is rare
- renal failure is unusual and seen in a minority of patients
Management
steroids/immunosuppressants (not shown to be useful)
A 20-year-old woman presents with a 5-day history of painless light brown coloured urine. She has experienced 3 episodes of this over the 5 days. There is no dyspareunia, urgency or pain elsewhere. As of now, she is afebrile though she alludes to being ill with a respiratory infection around three weeks ago.
Urine dipstick revealed protein and blood.
What is the most likely diagnosis?
- Post streptococcus glomerulonephritis (PSGN)
- UTI
- Pyelonephritis
- Alport’s syndrome
- IgA nephropathy
The symptoms, previous illness and proteinuria point to PSGN. This is a delayed antibody-mediated disease following infection of the pharynx or skin causing nephritic syndrome. Pyelonephritis and a UTI would present differently including symptoms such as fever, dysuria and pain. Alport’s is characterised by haematuria, sensory hearing loss and ocular disturbances. IgA nephropathy would occur a few days after the respiratory infection rather than weeks.
Post-streptococcal glomerulonephritis typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes). It is caused by immune complex (IgG, IgM and C3) deposition in the glomeruli. Young children are most commonly affected.
Features:
- headache
- malaise
- visible haematuria
- proteinuria
- this may result in oedema
- hypertension
- oliguria
- bloods:
- low C3
- raised ASO titre
IgA nephropathy and post-streptococcal glomerulonephritis are often confused as they both can cause renal disease following an URTI
Renal biopsy features
- post-streptococcal glomerulonephritis causes acute, diffuse proliferative glomerulonephritis
- endothelial proliferation with neutrophils
- electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
- immunofluorescence: granular or ‘starry sky’ appearance
A 3-year-old girl is brought to surgery as her parents have noticed blood in her urine. Examinations reveals a loin mass. MSU shows no evidence of a urinary tract infection. The only relevant family history is her grandmother who has chronic kidney disease.
A.Transitional cell carcinoma of the bladder
B.Renal stones
C.Benign prostatic hyperplasia
D.Wilms’ nephroblastoma
E.Urinary tract infection
F.Renal cell carcinoma
G.Polycystic kidney disease
H.Goodpasture’s syndrome
I.Rhabdomyosarcoma
J.Renal vein thrombosis
Wilms’ nephroblastoma is one of the most common childhood malignancies. It typically presents in children under 5 years of age, with a median age of 3 years old.
Features
- abdominal mass (most common presenting feature)
- flank pain
- painless haematuria
- other features: anorexia, fever
- unilateral in 95% of cases
- metastases are found in 20% of patients (most commonly lung)
You are bleeped by a nurse in the evening who you asks you to urgently review a 68-year-old lady who is two days post-op because her afternoon blood results have just been reported as being abnormal. You have never met the patient before and are not aware of their clinical course. She tells you the results are as follows:
Hb 146 g/l
Na+ 139 mmol/l
Platelets 159 * 109/l
K+ 6.1 mmol/l
WBC 13 * 109/l
Urea3.4 mmol/l
CRP 21 mg/l
Creatinine 73 µmol/l
You are unable to come to the ward for 10 minutes. What should you ask the nurse to do before you get there?
- 12 lead ECG
- Give calcium gluconate
- 15 ml by slow IV injection
- Blood culture
- Administer 10 U Actrapid in 50 ml of 50% glucose over 10 minutes
- Bleep the surgical registrar on call for a review
The British National Formulary (BNF) management of hyperkalaemia is as follows:
If K+ > 6.5 mmol/l or if there are ECG changes:
- Administer calcium gluconate 10% 10-20ml by slow IV injection titrated to ECG response
- Give 10 U Actrapid in 50 ml of 50% glucose over 10-15 minutes
- Consider use of nebulised salbutamol
- Consider correcting acidosis with sodium bicarbonate infusion
Management of hyperkalaemia, BNF, June 2016
Given that the patient’s K+ is only 6.1 at the moment, an ECG would be the first thing to do. It would also be sensible to repeat the K+ reading, probably with a venous blood gas but an ECG would reveal whether there was an immediate danger which needs treatment. After arriving on the ward it would be important to conduct a full clinical assessment of the patient including reading their notes and noting recent observations. Following this a blood culture or discussion with the surgical registrar may well be sensible options but you should do the basics of an ECG and rechecking the potassium first.
Untreated hyperkalaemia may cause life-threatening arrhythmias. Precipitating factors should be addressed (e.g. acute renal failure) and aggravating drugs stopped (e.g. ACE inhibitors). Management may be categorised by the aims of treatment
Stabilisation of the cardiac membrane
- intravenous calcium gluconate does NOT lower serum potassium levels
- Short-term shift in potassium from extracellular to intracellular fluid compartment
- combined insulin/dextrose infusion
- nebulised salbutamol
- Removal of potassium from the body
- calcium resonium (orally or enema)
- enemas are more effective than oral as potassium is secreted by the rectum
- loop diuretics
- dialysis
- haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia
A 71 year old woman has a 7 day history of vomiting and diarrhoea.
Bloods:
Na+143 mmol/l
K+5.7 mmol/l
Urea13 mmol/l
Creatinine325 mmol/l
Renal function was noted to be normal on routine blood tests one month ago. Which of the following is most consistent with a diagnosis of acute tubular necrosis?
- Low urinary sodium
- Postural drop of >20 mmHg
- Hydronephrosis on renal ultrasound
- Raised urinary osmolality
- Raised urinary sodium
This patient has acute kidney injury. The causes can be divided as follows:
Pre-renal:
- Caused by inadequate renal perfusion e.g. dehydration, haemorrhage, heart failure, sepsis
- Kidneys act to concentrate urine and retain sodium - urine osmolality high, urine sodium low
Renal:
- Most common = acute tubular necrosis
- Damage to tubular cells due to prolonged ischaemia or toxins
- Kidneys can no longer concentrate urine or retain sodium - urine osmolality low, urine sodium high
- Rarer causes = acute glomerulonephritis, acute interstitial nephritis
Post-renal:
- Obstruction of urinary tract
- Usually identified with hydronephrosis on renal ultrasound
- Extrinsic causes include pelvic malignancy and retroperitoneal fibrosis
Name the 3 NICE Criteria for Dx of AKI
a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than 8 hours in children and young people
a 25% or greater fall in eGFR in children and young people within the past 7 days.
Describe the management of AKI
- IV Fluids
- Stop Nephrotoxic Drugs (NSAIDs and ACE-Is)
- Relieve obstruction (catheterise/nephrostomy/urological intervention)
Name 3 Complications of AKI
- Hyperkalaemia
- Fluid Overload (HF/PO)
- Metabolic Acidosis
- Uraemia (encephalopathy/pericarditis)
Name 2 Investigations for AKI
Urinalysis for protein, blood, leucocytes, nitrites and glucose.
- Leucocytes and nitrites suggest infection
- Protein and blood suggest acute nephritis (but can be positive in infection)
- Glucose suggests diabetes
US of the urinary tract is used to look for obstruction. It is not necessary if an alternative cause is found for the AKI.
Think about a diagnosis of acute nephritis and referral to the nephrology team when an adult, child or young person with no obvious cause of acute kidney injury has urine dipstick results showing haematuria and proteinuria, without urinary tract infection or trauma due to catheterisation.
What are the main features of Nephritic Syndrome?
- Haematuria
- Proteinuria
- Fluid Retention
- Oliguria
What are the main features of Nephrotic Syndrome?
- Proteinuria
- Periperhal Oedema (Orbital/Ankle)
- Hypoalbuminaemia (serum)
- Hypercholesterolaemia
Name the 6 main types of Nephritic GN in order of most common
IgA Nephropathy (Berger’s)
Post-Strep GN
Membranous GN
Anti-GBM (Goodpasture’s)
HSP
Rapidly Progressive GN (RPGN)
Name the 4 main types of Nephritic GN in order of most common to least common
Minimal Change Disease
Focal Segmental Glomerulosclerosis (FSGS)
Membranous Nephropathy
Membranoproliferative GN
Name the main treatment of glomerulonephritis
- Immunosuppresion - steroids
- BP control - ACE-Is and ARBs
- Cyclophosphamide - indicated in RPGN
- Plasma Exchange (plasmophoresis) - anti-GBM
EACDIT of Haemolytic Uraemic Syndrome (HUS)
E
- Children <5yrs following contaminated food/water or outbreaks
A
- Classically Shiga Toxin-producing Escherichia Coli (STEC) 0157:H7 (‘verotoxigenic’, ‘enterohaemorrhagic’). This is the most common cause in children, accounting for over 90% of cases.
- Pneumococcal infection
Ix
- Full blood count: Normocytic anaemia, Thrombocytopaenia (low platelets), fragmented blood film
- U&E: acute kidney injury
- stool culture
- looking for evidence of STEC infection
- PCR for Shiga toxins
C
Usually presents in young children individuals, following diarrhoea - often bloody (~5d) with a triad of:
- AKI (due to thrombosis of glomerulus capillaries)
- Microangiopathic haemolytic (normocytic) anaemia (<100g/l)
- Thrombocytopenia (reduced platelets)
DDx
- TTP - generally presents with neurological signs (headache, fever, confusion)
- SLE
- DIC
- HELLP Syndrome
- Pre-eclampsia
Tx
- Supportive e.g. Fluids, blood transfusion and dialysis if required
- No role for antibiotics, despite the preceding diarrhoeal illness in many patients
- As a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
- Eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
- Avoidance of antibiotics, antimotility agents, and NSAIDs is advised.
EACDIT of Thrombocytopenic Thrombotic Purpura (TTP)
E
- Rare, typically adult females
A
Primary Causes
- ADAMS13 Deficiency (enzyme responsible for cleavage of VWF)
- VWF multimers form - platelets clump within vessels
Secondary Causes
- post-infection e.g. urinary, gastrointestinal
- pregnancy
- drugs: ciclosporin, oral contraceptive pill, penicillin, clopidogrel, aciclovir
- tumours
- SLE
- HIV
Ix
- FBC
- Clotting Factors
C
Pentad of (not all will be present)
- Fever
- Fluctuating neuro signs (microemboli)
- Microangiopathic haemolytic anaemia
- Thrombocytopenia
- Renal failure
Tx
- Plasma Exchange
- Corticosteroids
Give 4 main causes of CKD
- Diabetes
- Hypertension
- Age-related decline
- Glomerulonephritis
- Polycystic kidney disease
- Medications such as NSAIDS, proton pump inhibitors and lithium
Give 4 main RFs for CKD
- Older age
- Hypertension
- Diabetes
- Smoking
- Use of medications that affect the kidneys
Describe the presenting clinical features of CKD
Usually chronic kidney disease is asymptomatic and diagnosed on routine testing. A number of signs and symptoms might suggest chronic kidney disease:
- Pruritus (itching)
- Loss of appetite
- Nausea
- Oedema
- Muscle cramps
- Peripheral neuropathy
- Pallor
- Hypertension
Give 3 Investigations for CKD
- Estimated glomerular filtration rate (eGFR) can be checked using a U&E blood test. Two tests are required 3 months apart to confirm a diagnosis of chronic kidney disease.
- Proteinuria can be checked using a urine albumin:creatinine ratio (ACR). A result of ≥ 3mg/mmol is significant.
- Haematuria can be checked using a urine dipstick. A significant result is 1+ of blood. Haematuria should prompt investigation for malignancy (i.e. bladder cancer).
- Renal ultrasound can be used to investigate patients with accelerated CKD, haematuria, family history of polycystic kidney disease or evidence of obstruction.
Briefly describe the CKD Staging System
The G score is based on the eGFR:
- G1 = eGFR >90
- G2 = eGFR 60-89
- G3a = eGFR 45-59
- G3b = eGFR 30-44
- G4 = eGFR 15-29
- G5 = eGFR <15 (known as “end-stage renal failure”)
The A score is based on the albumin:creatinine ratio:
- A1 = < 3mg/mmol
- A2 = 3 – 30mg/mmol
- A3 = > 30mg/mmol
The patient does not have CKD if they have a score of A1 combined with G1 or G2. They need at least an eGFR of < 60 or proteinuria for a diagnosis of CKD.
Give some examples of complications of CKD
- Anaemia
- Renal bone disease
- Cardiovascular disease
- Peripheral neuropathy
- Dialysis related problems
When should CKD be referred to a specialist?
NICE suggest referral to a specialist when there is:
- eGFR < 30
- ACR ≥ 70 mg/mmol
- Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year
- Uncontrolled hypertension despite ≥ 4 antihypertensives
Describe the main management of CKD
Aims of management
- Slow the progression of the disease
- Reduce the risk of cardiovascular disease
- Reduce the risk of complications
- Treating complications
Slowing the progression of the disease
- Optimise diabetic control
- Optimise hypertensive control
- Treat glomerulonephritis
Reducing the risk of complications
- Exercise, maintain a healthy weight and stop smoking
- Special dietary advice about phosphate, sodium, potassium and water intake
- Offer atorvastatin 20mg for primary prevention of cardiovascular disease
Treating complications
- Oral sodium bicarbonate to treat metabolic acidosis
- Iron supplementation and erythropoietin to treat anaemia
- Vitamin D to treat renal bone disease
- Dialysis in end stage renal failure
- Renal transplant in end stage renal failure
- Mineral bone disease; low vitamin D and hyperphosphataemia. ‘Drags’ calcium from bones resulting in osteomalacia. Low Ca results in secondary hyperparathyroidism.
- Managed by reducing intake of phosphate (1st line), phosphate binders (sevelamer), Vitamin D (alfacalcidol/calcitrol) and in some cases parathyroidectomy. Alendronic acid can be used to help slow disease progression.
Describe the main treatment of CKD
ACE inhibitors are the first line in patients with chronic kidney disease. These are offered to all patients with:
- Diabetes plus ACR > 3mg/mmol
- Hypertension plus ACR > 30mg/mmol
- All patients with ACR > 70mg/mmol
Aim to keep blood pressure <140/90 (or < 130/80 if ACR > 70mg/mmol).
Serum potassium needs to be monitored as CKD and ACE inhibitors both cause hyperkalaemia.
Describe EACIT of Anaemia of CKD
- Healthy kidney cells produced erythropoietin. Erythropoietin is the hormone that stimulates production of red blood cells. Damaged kidney cells in CKD cause a drop in erythropoietin. Therefore there is a drop in red blood cells and a subsequent anaemia.
- Anaemia can be treated with erythropoiesis stimulating agents such as exogenous erythropoeitin. Blood transfusions should be limited as they can sensitise the immune system (“allosensitisation”) so that transplanted organs are more likely to be rejected.
- Iron deficiency should be treated before offering erythropoetin. Intravenous iron is usually given, particularly in dialysis patients. Oral iron is an alternative.
Describe the main features of Renal Bone Disease/CKD-Mineral and Bone Disorder
Features
- Osteomalacia (softening of bones)
- Osteoporosis (brittle bones)
- Osteosclerosis (hardening of bones)
Xray Changes
Spine xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white). This is classically known as “rugger jersey” spine after the stripes found on a rugby shirt.
Pathophysiology
- High serum phosphate occurs due to reduced phosphate excretion. Low active vitamin D because the kidney is essential in metabolising vitamin D to its active form. Active vitamin D is essential in calcium absorption from the intestines and kidneys. Vitamin D also regulates bone turnover.
- Secondary hyperparathyroidism occurs because the parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone. This leads to increased osteoclast activity. Osteoclast activity lead to the absorption of calcium from bone.
- Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.
- Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised.
- Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.
Describe the Management of Renal Bone Disease
Management involves a combination of:
- Active forms of vitamin D (alfacalcidol and calcitriol)
- Low phosphate diet
- Bisphosphonates can be used to treat osteoporosis
What are the main RFs for AKI?
Consider the possibility of an AKI in patients that are suffering with an acute illness such as infection or having a surgical operation. Risk factors that would predispose them to developing acute kidney injury include:
- Chronic kidney disease
- Heart failure
- Diabetes
- Liver disease
- Older age (above 65 years)
- Cognitive impairment
- Nephrotoxic medications such as NSAIDS and ACE inhibitors
- Use of a contrast medium such as during CT scans
AKI Management
Prevention of acute kidney injury is important. This is achieved by avoiding nephrotoxic medications where possible and ensuring adequate fluid input in unwell patients, including IV fluids if they are not taking enough orally.
The first step to treating an acute kidney injury is to correct the underlying cause:
- Fluid rehydration with IV fluids in pre-renal AKI
- Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
- Relieve obstruction in a post-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate
In a severe acute kidney injury or where there is doubt about the cause or complications, input from a renal specialist is required. They may need dialysis.
Describe the general features of Haemolytic Uraemic Syndrome (HUS)
Haemolytic uraemic syndrome (HUS) occurs when there is thrombosis in small blood vessels throughout the body. This is usually triggered by a bacterial toxin called the shiga toxin. It leads to the classic triad of:
- Haemolytic anaemia
- Acute kidney injury
- Low platelet count (thrombocytopenia)
The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood clots within the small vessels chop up the red blood cells as they pass by (haemolysis), causing anaemia. The blood flow through the kidney is affected by the clots and damaged red blood cells, leading to acute kidney injury.
The most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin and can cause HUS. The use of antibiotics and anti-motility medications such as loperamide to treat the gastroenteritis increase the risk of developing HUS.
Describe the clinical presentation of HUS
E. coli 0157 causes a brief gastroenteritis often with bloody diarrhoea.
Around 5 days after the diarrhoea the person will start displaying symptoms of HUS:
- Reduced urine output
- Haematuria or dark brown urine
- Abdominal pain
- Lethargy and irritability
- Confusion
- Hypertension
- Bruising
Describe the management of HUS
HUS is a medical emergency and has up to 10% mortality. The condition is self limiting and supportive management is the mainstay of treatment:
- Antihypertensives
- Blood transfusions
- Dialysis
70-80% of patients make a full recovery.
Maintenance fluid recommendations
Normal maintenance fluid recommendations:
- 25-30 ml/kg/day of water and
- approximately 1 mmol/kg/day of potassium, sodium and chloride
- approximately 50-100 g/day of glucose to limit starvation ketosis
Consider prescribing less fluid (for example, 20–25 ml/kg/day fluid) for patients who:
- are older or frail
- have renal impairment or cardiac failure
- are malnourished and at risk of refeeding syndrome (see Nutrition support in adults [NICE clinical guideline 32]).
CKD Staging
<90 ml/min with evidence of renal damage indicates CKD.
