Nephrology and Urology Flashcards
What is creatinine?
A waste product from muscle and protein metabolism.
Serum creatinine is a good marker of what?
Kidney function.
Why is serum creatinine a good marker of kidney function?
Creatinine is excreted by the kidneys. If filtration in the kidney is deficient serum creatinine concentrations rise.
Define acute kidney injury (AKI).
Reduction in renal function following an insult to the kidneys.
What are four clinical features of acute kidney injury?
Reduced urine output, pulmonary oedema, peripheral oedema and arrhythmias.
What are the three categories of causes of acute kidney injury?
Prerenal (ischaemic).
Intrinsic.
Postrenal (obstructive).
What are two pre-renal causes of AKI?
Hypovolaemia (secondary to diarrhoea and vomiting).
Renal artery stenosis.
What are five intrinsic causes of AKI?
Glomerulonephritis. Acute tubular necrosis. Acute interstitial nephritis. Rhabdomyolysis. Tumour lysis syndrome.
What are three post-renal causes of AKI?
Kidney stone in ureter or bladder.
Benign prostatic hyperplasia.
External compression of the ureter.
What two measurements are used to stage the severity of AKI?
Serum creatinine.
Urine output.
How is stage 1 AKI defined?
1.5x rise in serum creatinine from baseline (in the past 7 days).
Urine output < 0.5ml/kg/hour for six hours.
How is stage 2 AKI defined?
2-3x rise in serum creatinine from baseline (in the past 7 days).
Urine output < 0.5ml/kg/hour for at least twelve hours.
How is stage 3 AKI defined?
More than 3x rise in serum creatinine from baseline (in the past seven days).
Urine output < 0.3ml/kg/hour for 24 hours // Anuria for twelve hours.
How is AKI managed?
Supportive therapy. Fluid balance (ensure kidneys perfused without causing fluid overload).
Give examples of four classes of drug that should be stopped in AKI as they will worsen renal function.
NSAIDs, ACE inhibitors, ARBs and diuretics.
Give examples of three drugs that should be stopped in AKI as they may become toxic.
Metformin, lithium and digoxin.
What is renal artery stenosis?
Narrowing of the lumen of the renal artery (suppling the kidney).
What is main feature of renal artery stenosis?
Refractory hypertension.
Why does renal artery stenosis result in hypertension?
Reduced blood flow to the kidneys leads to activation on the RAAS… leading to an increase in blood pressure.
How does renal artery stenosis result in kidney damage?
Reduced blood flow to the kidneys leads to reduced glomerular filtration rate… leading to atrophy and fibrosis.
What investigations may be ordered in the diagnosis of renal artery stenosis?
Serum creatinine.
Duplex ultrasonography.
CT/MR angiography.
What does serum creatinine reveal in patients with renal artery stenosis?
Raised creatinine.
What is the pharmacological management of renal artery stenosis?
Captopril (ACEi).
Furosemide (thiazide diuretic).
Statin.
What is the long term (surgical) management option of renal artery stenosis?
Renal artery stenting.
What is glomerulonephritis?
The umbrella term for pathology affecting the glomerulus of the kidney. Spectrum of nephrosis to nephritis.
What is the characteristic triad of nephrotic syndrome?
Proteinuria, hypoalbuminaemia and oedema.
Other than the characteristic triad, what other features can be found on investigation in people with nephrotic syndrome?
Hyperlipidaemia.
Why do patients with nephrotic syndrome have hyperlipidaemia?
Low albumin = low oncotic pressure which prompts increased hepatic protein synthesis (including of lipoproteins).
What are complications of nephrotic syndrome?
Thrombosis, infections, cardiovascular complications, anaemia, acute renal failure, hypovolaemic crisis.
Why does nephrotic syndrome predispose to thrombosis?
Loss of antithrombin-III, proteins C and S.
What is the most common cause of nephrotic syndrome in children?
Minimal change disease.
How does minimal change disease present?
Periorbital/genital oedema, ascites and shortness of breath.
What is the pathophysiological process behind minimal change disease?
T-cell and cytokine-mediated damage to glomerular basement membrane. Polyanion loss and reduction in electrostatic charge. Increased glomerular permeability to serum albumin.
What investigation is indicated in patients suspected of minimal change disease?
Biopsy with electron microscopy.
What does biopsy with electron microscopy reveal in patients with minimal change disease?
Effacement of podocyte foot processes.
Where does minimal change disease get its name from?
Investigation with light microscopy appears normal.
What is the management of minimal change disease?
Corticosteroids.
In steroid-resistant cases give cyclophosphamide.
How should predisposition to thrombosis in nephrotic syndrome be treated?
Low molecular weight heparin (dalteparin).
What is focal segmental glomerulosclerosis?
A non-proliferative glomerulonephritis that causes nephrotic syndrome. Characterised by sclerosis of segments of some glomeruli and fusion of podocyte foot processes.
Focal segmental glomerulosclerosis (FSG) can be primary (idiopathic) or secondary. What are two causes of secondary FSG?
HIV and heroin use.
What investigation is indicated in patients suspected of focal segmental glomerulosclerosis?
Biopsy and light microscopy.
What does biopsy with light microscopy reveal in patients with focal segmental glomerulosclerosis?
Focal and segmental sclerosis and hyalinosis.
What is the management of focal segmental glomerulosclerosis?
Restricted salt intake, blood pressure control (w/ ACEi, ARB), loop diuretic (furosemide) and corticosteroids (in idiopathic disease).
What is membranous glomerulonephritis?
Slow progressive form of glomerulonephritis that causes nephrotic syndrome.
Membranous glomerulonephritis (MG) can be primary (idiopathic) or secondary. What are four secondary causes of MG?
Malignancy, infection, immunological disease, drugs.
What investigation is indicated in patients suspected of membranous glomerulonephritis?
Biopsy.
What does biopsy reveal in patients with membranous glomerulonephritis?
Spikes on silver staining.
What is the management of membranous glomerulonephritis?
Restrict salt intake, control blood pressure (w/ ACEi, ARB), loop diuretic (furosemide). In those at high risk of progression give corticosteroids and cyclophosphamide.
What are the four characteristic features of nephritic syndrome?
Haematuria, proteinuria, oliguria and hypertension.
What is nephritic syndrome?
Proliferative form of glomerulonephritis marked by an increased number of cells in the glomerulus.
What are three causes of nephritic syndrome?
IgA nephropathy.
Post-Strep glomerulonephritis.
Membranoproliferative glomerulonephritis.
What are three causes of nephrotic syndrome?
Minimal change disease.
Focal segmental glomerulonephritis.
Membranous glomerulonephritis.
What is IgA nephropathy glomerulonephritis?
The commonest form of primary glomerulonephritis in high-income countries.
Describe the pathophysiology of IgA nephropathy glomerulonephritis.
Develops several days after an upper respiratory tract infection because of IgA deposits in the space between glomerular capillaries.
How does IgA nephropathy glomerulonephritis present?
Features include visible haematuria, low grade proteinuria and hypertension.
How is IgA Nephropathy glomerulonephritis managed?
Conservatively in most cases though some will require antihypertensives (ACEi, ARB).
What is post-Strep glomerulonephritis?
Glomerulonephritis that develops three weeks after an upper respiratory tract infection.
How does post-Strep glomerulonephritis present?
Gross haematuria, oliguria, oedema.
How is post-Strep glomerulonephritis managed?
Supportively.
What is membranoproliferative glomerulonephritis associated with?
Hepatitis C and autoimmune conditions like SLE.
What does biopsy and light microscopy reveal in a patient with membranoproliferative glomerulonephritis?
Thickened glomerular basement membrane and tram-track appearance.
How is membranoproliferative glomerulonephritis managed?
Managed blood pressure (w/ ACEi, ARB).
What is the most common intrinsic cause of AKI?
Acute tubular necrosis.
What is acute tubular necrosis?
Damage to tubular cells from prolonged ischaemia or the presence of toxins.
What investigations are performed in patients with suspected acute tubular necrosis?
Urinary sodium.
Urine osmolality.
What do urinary sodium and urine osmolality reveal in a patient with acute tubular necrosis?
High urinary sodium and low urine osmolality.
What investigation finding is pathognomic for acute tubular necrosis?
Muddy brown casts.
What are three ischaemic causes of acute tubular necrosis?
Shock, sepsis, dehydration.
What are three toxic causes of acute tubular necrosis?
Radiology contrast dye, gentamicin, NSAIDs.
How is acute tubular necrosis managed?
Provide intravenous fluid and stop nephrotoxic medications.
What is the prognosis for acute tubular necrosis?
Epithelial cells have the ability to regenerate therefore ATN is reversible. Usually takes 7-21 days to recover.
What is acute interstitial nephritis?
A condition of inflammation of the space between cells and tubules (the interstitium) of the kidney.
What are the most common causes of acute interstitial nephritis?
Penicillin, rifampicin, NSAIDs, allopurinol and furosemide.
How does acute interstitial nephritis present clinically?
Fever, rash and arthralgia.
What investigations are performed on a patient suspected of acute interstitial nephritis?
Full blood count.
Urea and electrolytes.
Blood pressure.
Urinalysis.
What are the findings on investigation of acute interstitial nephritis?
Eosinophilia.
Renal impairment.
Hypertension.
White cells on urinalysis.
How is acute interstitial nephritis managed?
Treat underlying cause and consider giving steroids.
What is haemolytic uraemic syndrome?
A condition that occurs as a result of thrombosis in small blood vessels throughout the body.
Describe the pathophysiology of haemolytic uraemic syndrome.
Thrombosis consumes platelets (thrombocytopenia). Clots damage red blood cells causing haemolysis (anaemia). Blood supply to kidneys disrupted (AKI).
What is rhabdomyolysis?
Condition of skeletal muscle breakdown.
What causes rhabdomyolysis?
Underuse (prolonged immobilisation for many hours following a fall).
Overuse (prolonged epileptic seizure).
Trauma.
Rhabdomyolysis: what four things are released from myocytes when they undergo apoptosis?
Myoglobin.
Potassium.
Phosphate.
Creatine kinase.
What are the clinical features of rhabdomyolysis?
Muscle swelling and tenderness, fatigue, urine discolouration.
What investigations are performed in a patient suspected of rhabdomyolysis?
Creatinine (kidney function). Creatine kinase. Urinalysis. Serum phosphate. Serum potassium.
What does creatinine reveal in a patient with rhabdomyolysis?
Raised (acute kidney injury).
What does creatine kinase reveal in a patient with rhabdomyolysis?
Raised 10-100 times normal.
What does serum phosphate/potassium reveal in a patient with rhabdomyolysis?
Elevated phosphate.
Hyperkalaemia.
How is rhabdomyolysis managed?
Intravenous fluid.
Consider giving sodium bicarbonate to alkalinise urine.
What are the majority of renal stones made of?
Calcium oxalate.
What are the three main sites of renal stone deposition in the urinary tract?
Pelviureteric junction.
Pelvic brim.
Vesicoureteric junction.
Where do renal stones form?
Collecting ducts of the kidney.
How do renal stones present clinically?
Majority asymptomatic. Renal colic (loin to groin pain), nausea + vomiting, infection, haematuria, sterile pyuria, anuria.
What is the imaging investigation of choice for renal stones?
Non-contrast CT.
What pain relief is given for the management of renal stones?
Diclofenac.
What factor determines management of renal stones?
Size (< 5 mm likely to pass spontaneously).
When should renal stones be managed pharmacologically?
Size > 5 mm or if pain not resolving.
What pharmacological therapies can be used in the management of renal stones?
Nifedipine (CCB) or tamsulosin (alpha-blocker).
What is the next step in management if pharmacological intervention fails to resolve renal stones?
Extracorporeal shockwave lithotripsy… or later percutaneous nephrolithotomy.
What steps can be taken to reduce the risk of developing renal stones?
Lifestyle changes (high fluid intake, low animal protein, low salt diet). Thiazide diuretic use.
What are the three categories of urinary tract obstruction?
Luminal.
Mural.
Extra-mural.
Give examples of luminal lesions of urinary tract obstruction.
Stones, blood clot, sloughed papilla, tumour (renal, ureteric, bladder).
Give examples of mural lesions of urinary tract obstruction.
Congenital/acquired stricuture, neuromuscular dysfunction, schistosomiasis.
Give examples of extra-mural lesions of urinary tract obstruction.
Abdominal or pelvic mass/tumour, retroperitoneal fibrosis, iatrogenic.
What is the difference between the presentation of unilateral and bilateral urinary tract obstruction?
Unilateral obstruction may be clinically silent.
What is the clinical presentation of acute upper urinary tract obstruction?
Loin pain radiating to groin, possible superimposed infection with or without loin tenderness.
What is the clinical presentation of chronic upper urinary tract obstruction?
Flank pain, renal failure, superimposed infection, polyuria.
What is the clinical presentation of acute lower urinary tract obstruction?
Suprapubic pain, confusion, distended and palpable bladder.
What is the clinical presentation of chronic lower urinary tract obstruction?
Urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence with distended palpable bladder.
What is the imaging modality of choice for urinary tract obstruction?
Ultrasound.
If ultrasound confirms distension (urinary tract obstruction) what should be next step of investigation?
CT to determine level of obstruction.
Define hydronephrosis.
Dilatation of the renal pelvis and calyces.
Define pelviectasis.
Dilatation of the renal pelvis.
Define caliectasis.
Dilatation of the renal calyces.
Define hydroureter.
Dilatation of the ureter.
What is the management of upper urinary tract obstruction?
Nephrostomy or ureteric stent. Give tamsulosin to reduce stent-related pain.
What is the management of lower urinary tract obstruction?
Urethral or suprapubic catheters. Give tamsulosin if prostatic obstruction.
What % of men over 50 and 80 years old, respectively, have benign prostatic hyperplasia?
50% of men over 50.
80% of men over 80.
What is benign prostatic hyperplasia?
Noncancerous increase in size of the prostate gland.
What are the three groups of lower urinary tract symptoms?
Voiding symptoms (obstructive). Storage symptoms (irritative). Post-micturition symptoms.
Give examples of voiding symptoms of BPH?
Weak/intermittent urinary flow, straining, hesitancy, terminal dribbling, incomplete emptying.
Give examples of storage symptoms of BPH?
Urgency, frequency, urgency incontinence, nocturia.
Give an example of a post-micturition symptoms of BPH?
Dribbling.
What are two possible complications of benign prostatic hyperplasia?
Urinary tract infection.
Retention.
What pharmacological therapies can be used in the treatment of BPH?
Tamsulosin (alpha-blocker).
Finasteride (5 alpha-reductase inhibitor).
What is the mechanism of action of tamsulosin in the treatment of BPH?
Alpha-1 antagonist. Causes relaxation of smooth muscle of the bladder neck, prostate, ureter and urethra.
What is the mechanism of action of finasteride in the treatment of BPH?
5-alpha reductase inhibitor blocks conversion of testosterone to dihydrotestosterone, which is known to induce BPH.
What is the definitive management option for BPH?
Transurethral resection of prostate (TURP).
What is autosomal dominant polycystic kidney disease (ADPKD)?
The most common inherited cause of kidney disease. Characterised by the development of cysts which grow and compress the normal architecture and vasculature of the kidney.
What are the features of ADPKD?
Abdominal pain, abdominal masses, headaches, haematuria, hypertension, recurrent UTIs and renal stones.
Give examples of extra-renal manifestations of ADPKD?
Liver cysts, berry aneurysms, valvular heart disease, pancreatic cysts, splenic cysts.
How is ADPKD diagnosed?
Renal ultrasound along with CT KUB.
How is ADPKD managed?
Tolvaptan (decreases cell proliferation). Long term management is renal transplant.
Define chronic kidney disease (CKD).
Reduction in kidney function or structural damage present for at least three months, with associated health implications.
Over what period of time does CKD typically develop?
Months to years.
What are late signs of CKD?
Peripheral oedema, lethargy, nausea, loss of appetite, pruritus, muscle cramps and confusion.
What are four complications of CKD?
Cardiovascular disease.
Bone disease.
Anaemia.
Give five potential causes of CKD?
Diabetes mellitus. Hypertension. Glomerulonephritis. Polycystic kidney disease. Nephrotoxic drugs.
How is CKD diagnosed?
Calculation of estimated glomerular filtration rate (eGFR) and presence of albumin in the urine (proteinuria) on urinalysis.
What eGFR corresponds to severe reduction in kidney function?
< 30 ml/min.
What eGFR corresponds to established kidney failure?
< 15 ml/min.
How is CKD managed?
Blood pressure control with ACEi or ARBs. Further treatment with furosemide (loop diuretic) particularly if eGFR < 45.
What are side effects of furosemide?
Ototoxicity, hypokalaemia, dehydration, allergy, nephritis and gout.
How is phosphate excretion affected in chronic kidney disease?
Phosphate excretion is impaired and phosphate accumulates in the blood.
What is the affect of high serum phosphate levels on bone?
Phosphate drags calcium from the bones causing osteomalacia.
What investigation can be used to monitor bone health?
DEXA scans (measures bone mineral density).
What role do the kidneys have in the balance of vitamin D?
1-alpha hydroxylation (the process of converting calcifediol to calcitriol) occurs in the tubules of the kidneys.
How is vitamin D affected in chronic kidney disease?
Less active vitamin D is produced.
In CKD: how does low vitamin D affect calcium levels and why?
Vitamin D helps to increase absorption of calcium from the diet… therefore low serum calcium.
In CKD: low serum calcium can lead to the development of what two conditions?
Osteoporosis.
Secondary hyperparathyroidism.
What is the management of bone disease in CKD?
Reducing dietary intake of phosphate (avoid excessive meat, fish, dairy). Consider providing phosphate binders (aluminium salts, calcium carbonate) and vitamin D supplements. Give bisphosphonates (alendrotnic acid) to reduce the rate of bone turnover.
Why does CKD result in anaemia?
Erythropoietin is secreted by the kidneys that stimulates red blood cell production in the bone marrow. In CKD erythropoietin production release is impaired causing anaemia. In addition, uraemia has a toxic effect on the bone marrow which further reduces erythropoiesis.
What stimulates erythropoietin secretion by the kidneys?
Cellular hypoxia.
What is the management of anaemia in CKD?
If iron stores are insufficient give intravenous iron infusion. Ir iron stores are sufficient give erythropoietin/
What are the clinical features of renal failure?
Breathlessness, fatigue, insomnia, pruritus, poor appetite, oedema, weakness, abdominal cramps, anxiety and cognitive impairment.
What are the two management pathways for a patient with renal failure?
Palliative care or renal replacement therapy.
What are three types of renal replacement therapy?
Haemodialysis.
Peritoneal dialysis.
Renal transplantation.
Describe the process of haemodialysis.
Filtration of the blood through a dialysis machine in hospital, typically requires three sessions per week (each lasting three to five hours).
Describe the process of peritoneal dialysis.
Filtration occurs within the patient’s abdomen. Dialysis solution is injected into the abdominal cavity via a permanent catheter. The solution draws waste products from the blood across the peritoneum. After several hours of dwell time the solution is exchanged for a new solution.
In renal transplantation: what site is the donor kidney transplanted to?
The groin, renal vessels are connected to the external iliac vessels.
Following renal transplantation patients have an increased risk of what cancer and why?
Squamous cell carcinoma of the skin due to effects of long-term immunosuppressants.
