Renal pathology Flashcards
State the functions of the kidney.
- Endocrine function - prod of erythropoietin, renin, active 25-hydroxy vitamin D
- Reabsorb glucose, amino acids and bicarbonates
- Maintain balance of electrolytes, water & pH
- Control BP
- Excrete waste/excess products
(2,3,4,5 = homeostasis)
Define GFR.
What is the average GFR for a 70kg person?
The volume of fluid filtered from the glomeruli into Bowman’s space per unit time (minutes).
90 - 120 ml/min.
Why can albumin not pass through the filtration barrier?
The barrier is negatively charged, as is albumin.
What is creatinine? Define eGFR.
Creatinine = waste product of muscles. eGFR = Estimate of creatinine generation based on a patient's serum creatinine level, age, sex and race. Likely to be inaccurate in people at extremes of muscle mass e.g. severely malnourished, amputees, body builders, morbidly obese.
What area of the kidney is most vulnerable to ischaemic injury and what does this often result in?
PCT. Acute tubular necrosis.
What % of cardiac output does each kidney receive?
20%
1L/min.
Why does water flow out of the blood into Bowman’s space?
The afferent arteriole has a wider diameter than the efferent, thus pressure in glomerulus is high & water and solutes are forced out.
Why is potassium and hydrogen ion excretion imparied in hypotensive or hypovolaemic patients?
???
Renal perfusion is low thus glomerular filtration is also low, which means reabsorption of water and sodium by PCT increases so minimal fluid reaches DCT.
List some causes and signs of Fanconi syndrome.
A disorder of the PCT.
Causes: cytinosis, Wilson’s, Tenofovir drug (HIV)
Signs: aminoaciduria, glycosuria, phosphate wasting (resulting in rickets/osteomalacia), bicarbonate wasting/acidosis with failure of urine acidification.
What is the effect of hyperaldosteronism on electrolyte balance?
Excessive Na+ reabsorption resulting in a negative tubular fluid, K+ and H+ rush in to lumen = hypokalaemic alkalosis
What is the effect of Addison’s on electrolyte balance?
Hyperkalaemic acidosis. Corrected by giving sodium bicarb.
What 2 factors govern potassium reabsoprtion?
Distal delivery of Na+, aldosterone.
State 2 hormones that drive cellular K+ uptake.
Insulin, catecholamines (epinephrine). Do so by activating Na/KATPase pumps. Diabetic ke
State two types of medication that can cause hypokalaemia and the mechanism by which this occurs.
Loop diuretics (inhibit NKCC2 in thick ascending limb), thiazide diuretics (inhibit NCC in distal tubule). The inhibition of Na reabsorption results in greater delivery of sodium to the collecting duct, where enhanced Na influx through epithelial Na channels (eNac) results in potassium efflux, which can result in the development of hypokalemia. “Increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine. The increased hydrogen ion loss can lead to metabolic alkalosis. Part of the loss of potassium and hydrogen ion by loop and thiazide diuretics results from activation of the renin-angiotensin-aldosterone system that occurs because of reduced blood volume and arterial pressure. Increased aldosterone stimulates sodium reabsorption and increases potassium and hydrogen ion excretion into the urine.”
List types of medication that can cause hyperkalaemia.
Spironolactone (aldosterone antagonist) Amiloride (acts on eNac channels) ACE inhibitors Angiotensin receptor blockers (ARB)
Define acute kidney injury.
An abrupt (1-7 days) & sustained (>24 hrs) deterioration in renal function, usually reversible over days - weeks. Often recognised by a falling urine output and rising serum urea and creatinine, or both.
Briefly describe the pathophysiology of AKI.
Rapid decline in GFR, often due to decreased renal perfusion, leading to a failure to maintain fluid, electrolyte and acid-base homeostasis
Who is typically affected by AKI / how common is AKI?
Elderly, sepsis (25%), septic shock patients (50%).
18% of hospital patients and ~50% of ICU patients.
Incidence of community acquired AKI is 5% in UK.
Severe AKI affects 130-140 per million population per year.
Mortality rates for uncomplicated sepsis 5-10%, for severe 50-70%.
What 3 categories are the causes of AKI divided in to?
- Pre renal (40-70%) - reduced kidney perfusion leads to falling GFR.
- Renal (10-50%) - injury to glomerulus, tubules or vessels.
- Post renal (10-25%) - functioning kidneys cannot excrete urine due to urinary tract obstruction
What is the RIFLE criteria and what does it stand for?
Old system
Describes 3 levels of renal function (RIF) defined by serum creatinine or urine output, and 2 outcome measures (LE) defined by the duration of loss of fxn. Indicates an increasing degree of renal damage and mortality value as you go down the letters.
Risk, Injury, Failure, Loss, End stage renal disease.
What is the system currently used to diagnose AKI?
KDIGO system. Like RIFLE criteria it uses serum creatinine and urine output to assess severity. Only one criterion (SCr or urine output) has to be fulfilled to qualify for a stage
Stages 1-3. Stage 1:
• Rise in creatinine >1.5x baseline* within 7 days or >26.5μmol/L in 48hrs
• Urine output < 0.5mL/kg/h for >6 consecutive hours
*Baseline = best fig in last 6 months.
State the causes of prerenal AKI.
Hypoperfusion either due to falling circulating volume:
- Hypovolaemia (e.g. due to dehydration, haemorrhage)
- Hypotension without hypovolaemia e.g. cirrhosis, septic shock
- low cardiac output e.g. cardiac failure, cardiogenic shock
or intrarenal vasomotor changes that drop glomerular perfusion pressure:
-NSAIDs (inhibit production of renal prostoglandins by COX 1 & 2, pglandins dilate afferent arteriole)
-ACE inhibitors
(nephrotoxins)
State the causes of intrinsic/renal AKI.
Renal parenchyma damage due to:
- 80-90% due to acute tubular necrosis (e.g. due to prerenal damage & nephrotoxins like NSAIDs, uric acid crystals, myeloma, increased Ca2+, also due to
- Vascular damage: renal artery/vein thrombosis, emboli, vasculitis, haemolytic anaemia, haemolytic uraemic syndrome (HUS)
- Glomerular damage: glomerulonephritis, SLE
- Interstitial damage: infiltration with lymphoma, infection, tumour lysis following chemo
State the causes of post renal AKI.
Urinary tract obstruction at ureter, bladder or prostate due to
- Luminal: stones, clots
- Mural (wall): malignancy, BPH
- Extrinsic compression from malignancy esp from pelvis or retroperitoneal fibrosis
How can pre renal AKI be distinguished from renal AKI using biochemical markers?
Prerenal AKI shows higher urine osmolality and lower urine sodium due to salt retention.
Renal AKI may be indicated by immunoglobulins, paraproteion, autoantibodies.
What are the risk factors for AKI?
-Age>75yrs
-Male sex
Comorbidities:
-Cardiovasc disease (heart failure, peripheral vascular disease)
-Chronic liver disease i.e. cirrhosis
-Diabetes M
How does AKI present clinically?
- On examination there may be palpable bladder, palpable kidneys (polycystic disease)
- Loin & groin pain
- Oliguria
- Symptoms of uraemia: weakness, fatigue, anorexia, nausea, vomiting, mental confusion, seizures, coma
- Breathlessness from a combination of anaemia and pulmonary oedema secondary to impaired fluid excretion/volume overload
- Pericarditis occurs with severe untreated uraemia and may be complicated by a pericardial effusion, tamponade or pericardial rub
- Impaired platelet function causes bruising and exacerbates GI bleeding
- Infection due to immune suppression
How does AKI present biochemically?
- hyperkalaemia –> arrhythmias
- metabolic acidosis (unless H+ ions are lost by vomiting which itself can be caused by acidosis)
- hyponatraemia (due to water overload from continued drinking in response to oliguria)
- hypocalcaemia (due to reduced vit D prod)
- hyperphosphataemia
State the 3 aims of investigation in AKI.
- To differentiate acute from chronic uraemia.
- To establish whether AKI is prerenal, renal or post.
- To establish the degree of renal impairment and obtain baseline values so that response to treatment can be monitored - measurement of serum urea and creatinine.
What investigations might you perform for suspected AKI?
- Blood count - anaemia & high ESR suggest myeloma or vasculitis
- Mid stream urine & blood cultures to exclude infection
- Urine dipstick - can suggest infection (leucocytes + nitrites) and intrinsic renal disease, spec glomerular disease (Haematuria/
proteinuria) - Urinary electrolytes to determine prerenal vs renal
- Serum Ca, Pi, and uric acid.
- Ultrasound - detect obstruction, assessment of renal size (very small indicates CKD), corticomedullary differentiation (reduced in CKD). CT is useful in detecting retroperitoneal fibrosis & other causes of obstruction (post renal.)
- Histological investigation: renal biopsy should be performed in every patient with unexplained AKI and normal sized kidneys.
How is AKI managed?
-In prerenal, treat hypovolaemia with fluids
-In postrenal, catheterise or if still obstructed consider cystoscopy and retrograde stent or nephrostomy insertion (buys time to allow treatment of cause of obstruction)
Common to all aetiologies of AKI:
-Fluid balance
-Hyperkalaemia:
• Insulin & glucose - drives K+ into cells
• Calcium gluconate - no effect on K levels but reduces the excitability of cardiomyocytes, lowering likelihood of cardiac arrhythmias (cardio protective)
-Treat acidosis with sodium bicarb
-Treat pulmonary oedema with diuretics e.g. furosemide or dialysis/
haemofiltration
-Diet: Na+ & K+ restriction, supply vitamin D
-Dialysis or haemofiltration
nephrotoxins
How is fluid balance optimised in hypovolemia?
- Examine before and after all fluid given to ensure an adequate response and to reduce the risk of overload.
1. Give 500mL crystalloid over 15 min.
2. Reassess fluid state. Get expert help if unsure or if patient remains shocked.
3. Further boluses of 250–500mL crystalloid with clinical review after each.
4. Stop when euvolaemic or seek expert help when 2L given.
State some causes of hypervolaemia and describe treatment?
Aggressive fluid resuscitation, oliguria, and in sepsis due to increased capillary
permeability.
-Monitor weight daily in patients receiving IV fluids. Treat with:
• Oxygen supplementation if required.
• Fluid restriction. Consider oral and IV volumes. Give antibiotics in minimal fluid
and consider concentrated nutritional support preparations.
- Diuretics. Only in symptomatic fluid overload. They are ineffective and potentially harmful if used to treat oliguria without fluid overload.
- Renal replacement therapy (p306). AKI with fluid overload and oligo/anuria needs urgent referral to renal/critical care.
Which ECG changes indicate hyperkalaemia?
Tall ‘tented’ T waves; increased PR interval; small or absent P wave; widened QRS complex; ‘sine wave’ pattern; asystole.
When is hyperkalaemia treated and how?
Treat K+ >6.5mmol/L or any with ECG changes (ECG for all K+ >6.0mmol/L)
1. Calcium chloride/calcium gluconate) IV via a
big vein over. This is
cardioprotective (for 30–60min) but does not treat K+
level.
2 IV insulin in glucose - stim intracellular uptake. Monitor hourly for hypoglycaemia which may be delayed in renal impairment.
3. Salbutamol also causes an intracellular K+ shift but high doses are required
(10–20mg via nebulizer) and tachycardia can limit use (10mg dose in IHD, avoid
in tachyarrhythmias).
4 Definitive treatment requires K+ removal. If the underlying pathology cannot
be corrected renal replacement may be indicated. Safe transfer to an off site
renal unit requires K+ <6.5mmol/L—discuss with renal team and critical care.
What are the indications for RRT in AKI?
- Persistent fluid overload or hyperkalaemia unresponsive to medical treatment.
- Refractory pulmonary oedema
- Severe/prolonged acidosis.
- Uraemic encephalopathy or pericarditis
- Drug overdose – BLAST ( Barbiturate, Lithium, Alcohol-ethylene glycol, Salicylate, Theophylline)
Haemofiltration is most commonly used but haemodialysis is also an option.
What are some risks of RRT?
Risks of dialysis catheter insertion and mainte-
nance: infection procedural hypotension, bleeding due to the requirement for anticoagula-
tion, altered nutrition and drug clearance.
When might you refer to a nephrologist?
- Hyperkalaemia or fluid overload unresponsive to medical treatment.
- Urea > 40mmol/L +/- signs of uraemia
- No obvious cause
- Creatinine > 300 or rising > 50micromol/L per day
Define acidosis in terms of pH levels.
Mild = pH 7.30–7.36 (~bicarbonate >20mmol/L).
• Moderate = pH 7.20–7.29 (~bicarbonate 10–19mmol/L).
• Severe = pH <7.2 (~bicarbonate <10mmol/L): refer to renal/critical care.
How is acidosis treated?
Treatment is of the underlying disorder which will stop acid production. Where effect of treatment may be delayed, acidosis will persist and RRT may be indicated.
Medical management is controversial: giving sodium bicarbonate will generate CO2. Adequate ventilation is therefore needed to prevent respiratory acido-
sis worsening the clinical picture. Sodium bicarbonate also represents a sodium and
a volume load which can precipitate fluid overload in the vulnerable patient.
Differential diagnosis of AKI?
Abdominal aortic aneurysm (AAA), alcohol toxicity, alcoholic & diabetic ketoacidosis, chronic renal failure, dehydration, GI bleed, heart failure, metabolic acidosis.
What is the prognosis for AKI?
Most common cause of death: sepsis as a result of impaired immune defence (from uraemia and malnutrintion) and intrsumentation (dialysis and urinary atheters and vascular lines).
AKI is irreversible in a few patients probably bc of cortical necrosis which heals with formation of scar tissue, unlike tubules that can regenerate.
Define chronic kidney disease.
Longstanding, usually progressive impairment in renal function (haematuria, proteinuria or anatomical abnormality) for more than 3 months, with health implications.
GFR < 60mL/min/1.73 m2 for more than 3 months with/without evidence of kidney damage (haematuria etc)
How common is CKD in the general population?
6-11%
Describe the epidemiology of CKD.
- risk increases with age thus incidence is rising as we are living longer
- more common in females
Why is screening recommended for patients at risk of CKD?
Early intervention can reduce progression to end-stage renal failure.
List some of the causes of CKD.
- Idiopathic – 20%
- Congenital/inherited:
- Polycystic kidney disease/any hereditary kidney disease
- Tuberous sclerosis
Glomerular:
-Primary glomerulonephritides e.g. IgA nephropathy
Primary glomerular disease: DM, amyloidosis, SLE
Vascular:
- Hypertensive nephrosclerosis (common in African black ppl)
- atherosclerotic renovascular disease
- Small and medium sized vessel vasculitis
Other:
- Diabetes M – type 2>type 1
- Hypertension
- Neoplasma
- Myeloma
- any causes of chronic urinary tract obstruction
What are the risk factors for CKD?
- Smoking
- Old age
- Hypertension
- Diabetes Mellitus
- CVD .e.g ischaemic heart disease
- AKI
- Renal stones
- BPH
- Recurrent UTI’s
- African, Afro-Caribbean or Asian origin
- Chronic use of NSAIDs
Why is CKD often asymptomatic in early stages?
The kidney has a lot of reserve capacity - each kidney has roughly 1 mil nephrons.
What are some clinical complications/signs & symptoms of CKD?
Renal:
- nocturia
- polyuria
- salt and water retention leading to odeoma
Anaemia (normochromic normocytic) due to reduced EPO prod:
-Pallor, lethargy, breathlessness on exercise. Increased blood loss from gut during haemodialysis may contribute.
Bone pain/disease due to renal phosphate retention and impaired vit D prod lead to fall in serum Ca thus increase in parathyroid (secondary hyperparathyroidism) --- skeletal decalcification. "Renal osteodystrophy" = -Osteoporosis -Osteomalacia -hyperparathrydoisim -Osteosclerosis
Neurological complications.
- CNS: advanced uraemia (toxic metabolic accumilation) causes depressed cerebral function e.g. confusion, fits, coma
- PNS:
- polyneuropathy manifests as peripheral parasthesia / weakness.
- autonomic dysfunction presents as postural hypotension and disturbed GI motility
- median nerve compression in carpal tunnel syndrome caused by amyloidosis (complication of dialysis).
- Several mechanisms involved include toxic metabolic accumulation, hyperkalemia, hypercoagulability, immunologic disturbances, and acid base disequilibrium.
CVS:
-pericarditis and pericardial effusion due to secer uraemia
-MI, cardiac failure, stroke due to hypertension, hyperlipidaemia and vascular calcification
Other:
-anoreixia and weight loss (GI)
-nausea, vomiting, diarrohea (GI)
-insomnia
-itching
-Pruritus due to nitrogenous waste products of urea
How can CKD be differentiated from AKI?
differential diagnosis
- history
- duration of symptoms
- normochromic anaemia, small kidneys and presence of renal osteodystrophy favour CKD.
Briefly describe the progressive nature of the pathophysiology of CKD.
In CKD, where many nephrons have failed, and scarred, the burden of filtration falls to fewer functioning nephrons.
These remnant nephrons experience increased flow per nephron (hyperfiltration), as blood flow has not changed, and adapt with glomerular hypertrophy and reduced arteriolar resistance.
Increased flow, increased pressure and increased shear stress set in motion a VICIOUS CYCLE of raised intraglomerular capillary pressure and strain, which accelerates remnant nephron failure.
-each kidney has roughly 1 mil nephrons.
What role does the RAAS play in CKD pathophysiology?
Reduced renal perfusion leads to decreased transglomerular pressure and decreased GFR.
The response is intrarenal activation of RAAS:
Angio 2:
-efferent arteriolar/postglomerular arteriole vasoconstriction to increase transglomerular pressure. GFR increases
-increases pore size between mesangial cells and podocytes thus impairing the size-selective function of the basement membrane for macromolecules e.g. protein - resulting in increased proteinuria
-modulates cell growth directly and indirectly by upregulating transforming growth factor-beta (TGF-Beta), a potent fibrogenic cytokine, increasing collagen synthesis and epithelial cell transdifferentiation to myofibroblasts that contribute to excessive matrix formation
-up regulates plasminogen activator inhibitor-1 (PAI-1), which inhibits matrix proteolysis by plasmin - resulting in the accumulation of excessive matrix and scarring in both the glomeruli and interstitium
What investigations would you perform in a case of suspected CKD?
Urinalysis:
- Early morn sample for (ACR)/(PCR)
- dipstick analysis for haematuria (indicated glomerulonephritis), proteinuria (if heavy suggests glomerular disease, can be caused by infection)
• Mid-stream urine sample sent for microscopy and sensitivity???
- Urine microscopy: • White cells - bacterial UTI • Eosinophilia - allergic tubulointerstitial nephritis/cholesterol emboli • Granular casts - active renal disease • Red cells - glomerulonephritis
-Bloods:
- Serum biochemistry
• Urea, electrolytes, bicarbonate and creatine - HIGH UREA & CREATININE, LOW Ca2+
• Low Hb
• Low eGFR
• Raised alkaline phosphatase (renal osteodystrophy)
• Raised PTH if CKD stage 3 or more
Immunology:
• Auto-antibody screening for SLE, scleroderma and Goodpastures • Hep B, C, HIV and streptococcal antigen tests
maging:
• Ultrasound to check renal size and exclude hydronephrosis
(obstruction & dilation of renal pelvis):
- In CKD kidneys tend to be small
- Can be large in infiltrative disorders e.g. amyloidosis
• CT:
- Detect stones, retroperitoneal fibrosis and other causes of urinary
obstruction and maybe cortical scarring
-Biopsy and histology to diagnose condition causing renal failure
What are the aims of treatment in CKD?
- Specific therapy aimed at underlying cause of renal disease
- Slow the deterioration of kidney function (renoprotection)
- Reduce cv risk
- Treat complications e.g. anaemia
- Dose adjustment of prescribed drugs based on national formulary guidance.
Describe how you would treat CKD in terms of renoprotection.
-goal is to maintain bp less than 12/80mmHg & urinary conc less than 0.3g/24 hrs
-stop smoking, weight loss
Patients with CKD and proteinurea > 1g/24 hrs:
-ACE inhib e.g. ramipril
-Angiotensin receptor agonist e.g. Candesartan if goals not achieved/if diabetic
-diuretic e.g. ORAL BENDROFLUMETHIAZIDE to prevent hyperkalaemia and help BP control
-calcium channel blocker e.g. verapamil if goals not achieved
Describe how you would treat CKD in terms of CVD.
- Control bp and proteinurea as described in renoprotection
- smoking cessation, weight loss
- normal protein diet (0.8-1g/kg body weight/day)
- Statins e.g. simvastatin to lower cholesterol
- give aspirin
- optimise diabetic control: HbA1c 53mmol/mol
Describe how you would treat CKD in terms of bone disease.
-check PTH, if raised:
Treat hyperphosphataemia:
-restrict diet to low phosphate e.g. avoid milk, cheese, eggs
-phosphate binders e.g. calcium carbonate to decrease gut absorption
-vitamin D analogues e.g. calcitriol and Ca2+ supplements
This will also treat hyperkalaemia.
How would you treat anaemia in CKD?
- iron/folate/folic acid
- recombinant human erythropoeitin (expensive, may lead to hypertension)
If a patient fails to respond to treatment for anaemia in CKD, what might this be due to?
- haematinic deficiency
- bleeding
- malignancy
- infection
What does acidosis in CKD contribute to and how would you treat acidosis?
- increased serum potassium, dsypnea, lethargy
- sodium bicarbonate
How would you treat oedema in CKD?
Furosemide.
What protective measures should be taken in patients with CKD?
Influenza and pneumococcal vacination bc more at risk of infections.
When might you refer a patient with CKD to a nephrologist?
- severe CKD: GFR<30mL/min/1.73m2
- rapidly deteriorating kidney function: fall in eGFR> 5mL/min in 1 yr or >10mL/min/year in 5 years
- high levels of protein urea: ACR ≥ 70mg/mmol or PCR ≥ 100mg/mmol
- Proteinurea & haematuria: proteinurea with ≥ +1 blood on urine dipstick
- Poorly controlled hypertension despite use of antihypertensives
- Suspected rare or genetic cause of CKD
How does haemodialysis work?
Blood in an extracorporeal circulation is exposed to dialysis fluid separated by an artificial semi permeable membrane. Uraemic toxins diffuse down the conc gradient from blood to dialysis fluid. The gradient is maintained by replacing ‘used’ dialysis fluid with fresh fluid.
Patients are anticoagulated with heparin bc contact of blood w foreign substances activates clotting cascade.
What are the requirements for haemodialysis?
Blood flow must be at least 200ml/min and is achieved by arteriovenous fistula which also provides permanent and easily accesible site for needle insertion.
Patient must be haemodynamically stable, not atherosclerotic, can’t have many fistulas.
What are some advantages and disadvantages of haemodialysis?
-good clearance of solutes in short periods
-time consuming
Complications may occur:
-hypotension
-nausea
-chest pain
-infected dialysis catheter
How does peritoneal dialysis work?
A permanent tube (Tenckhoff catheter) is placed into the peritoneal cavity via subcut channel. Bags of dialysite are connected and fluid runs into peritoneal cavity. Urea, creatinine, phosphate & other uraemic toxins pass into fluid down their conc gradients and fluid is drained out.
P dialysis is done at home.
What are some advantages and disadvantages of peritoneal dialysis?
More convenient than haemodialysis bc can be done at home without need for nurses.
Complications:
-infection e.g. peritonitis often with S. epidermidis
-abdominal wall herniation
-intestinal perforation
-loss of membrane function (peritoneum fxn) over time
How does haemofiltration work?
Plasma water is removed along with its dissolved constituents (Na, K, urea, phosphate) through a highly permeable membrane, and replaced with solution of desired biochemical composition.
What form of dialysis is most commonly used for treatment of CKD?
Peritoneal
What form of dialysis is most commonly used for treatment of AKI in the ICU setting?
HaemoFILTRATION.
What are some complications of all long term RRT?
- CVD (as a result of atheroma)
- Sepsis due to peritonitis complicating p dialysis, S.aureus infection including endocarditis complicating access to indwelling devices for haemodialysis
- Amyloidosis due to accum of beta 2 microglobulin which is normally removed by kidneys but not by dialysis membranes, can cause carpal tunnel syndrome, arthalgia, fractures.
- malignancy
What are the advantages and disadvantages of renal transplant?
- chance of complete rehabilitation
- doubles life expectancy, improves quality of life
- more cost effective than dialysis in long term
-donor must be ABO compatible
-long term immunosuppression e.g. corticosteroid such as prednisone + azathioprine + ciclosporin
Complications:
-opportunistic infection
-hypertension
-tumour developement
-recurrence of renal disease
What are renal caliculi (nephrolithiasis) and ureteral stones (urolithiasis) composed of?
Most stones: calcium oxalate (60%) and/or calcium phosphate (10%).
Also uric acid (10%), magnesium ammonium phosphate/struvite (10%), cystine (1%).
Which 3 narrowings are renal and ureteral stones most often found?
- pelviureteric junction
- pelvic brim
- vesicoureteric junction (where ureter meets bladder)
Describe the epidemiology of renal/ureteral stones.
- incidence is increasing
- 10% lifetime risk
- peak age 20-40
- male:female 2:1
- higher in middle east due to higher oxalate and lower ca diet, also increased risk of dehydration in hot climate
Why do renal/ureteral stones form?
The solute concentrations of normally soluble material e.g. calcium exceeds saturation, beginning the process of crystal formation.
What are some causes of renal/ureteral stone formation?
- Anatomical abnormalities e.g. horseshoe, duplex, spina bifida
- Hypercalcicuria/hypercalcaemia
- Polycystic kidney disease
- Hyperoxaluria
What are some causes of hypercalciuria leading to calcium stone formation?
- Hypercalcaemia (most commonly caused by hyperparathyroidism)
- Excessive dietary intake of calcium
- Excessive resorption of calcium from bone e.g. with prolonged immobilization
- Idiopathic hypercalcaemia: increased absorption of Ca from gut and in turn increased urinary excretion with normal serum calcium levels.
- Primary renal disease e.g. polycystic renal disease or renal tubular acidosis – alkaline urine favours precip of stones??
What are some causes of hyperoxaluria leading to calcium oxalate stone formation?
Increased oxalate excretion favours formation of calcium oxalate even if calcium excretion is normal.
- High oxalate dietary intake: e.g spinah, rhubarb, tea. Or low Ca dietary intake results in hyperoxaluria via decreased intentinal binding of oxalate by Ca thus increased oxalate absoprtion and urinary excretion.
- Enteric hyperoxaluria: chronic intestinal of any cause leads to reduced intestinal Ca for oxalate binding
- Primary hyperoxaluria: rare AR enzyme deficiency
What are some causes of uric acid/urate stone formation?
Hyperuricaemia e.g due to impaired excretion (CKD, hypertension) or increased production (increased purine turnover, myeloproliferative disorders e.g. polycythaemia vera).
Who is at risk of uric acid stone formation?
Patients with ileostomies bc loss of bicarbonate from GI secretions results in acidic urine and reduced solubility of uric acid.
Which UTI causing organisms are associated with struvite stones and how?
Proteus, Klebsiella and Pseudomonas.
They produce enzyme urease which hydrolyses urea to ammonia, raising urine pH. Alkaline urine and high ammonia favour stone formation.
What causes cystine stones?
Cystinuria due to AR conditon affecting cystine and other basic aa transport (lysine, arginine, ornithine) across luminal membrane of PCT and small intestine.
How do stones present clinically?
- Mostly asymptomatic
- Pain (loin, groin)
- Haematuria
- UTI
- UTO
Where are the stones that often cause renal colic found?
Ureteric stones - upper urinary tract obstruction.
How do ureteric stones often present?
Renal colic - a severe intermittent (comes and goes in waves as ureters peristalise) pain lasting for hours.
- Rapid onset
- Felt anywhere between loin and groin, may radiate to scrotum or labium or tip of penis.
- Associated w nausea, vomiting
- Haematuria
- Often can’t lie still (differentiates from peritonitis)
How do bladder stones often present?
Increased urinary frequency and haematuria.
How do urethral stones often present?
Bladder outflow obstruction resulting in anuria and painful bladder distension.
If infection is present in UTO what may this present as?
Acute pyelonephritis: fever, rigors, loin pain, nausea, vomiting.
What are some differentials for renal/ ureteric stones?
- Vascular accident e.g. rupture aortic abdominal aneurysm (AAA) if over 50
yrs - until proven otherwise - Bowel pathology e.g. diverticulitis or appendicitis
- Ectopic pregnancy or ovarian cyst torsion - do uric pregnancy test
- Testicular torsion - can present with loin pain and nothing else
-Bleeding within kidney e.g. after biopsy can prod clots that temporarily lodge in ureter causing ureteric colic
How would you take a history for a patient presenting with renal colic?
SOCRATES.
Site, onset, character, radiation, associated features, timing, exacerbating/relieving factors, severity.
What investigations would you do in a case of suspected renal/urinary tract stones?
-Detailed history - vit D consumption (leading to hypercalcaemia), recurrent UTI’s, intestinal resection, gout.
BOXES.
B: Serum urea, electrolyte, creatinine and calcium. FBC.
O: Chemical analysis of any stone passed. Urine dipstick to check for blood, red cells, protein etc. Mid stream urine specimen for culture. Urine preg test to exclude ectopic pregnancy.
X: NCCT-KUB is the 1st line and best diagnostic test available - no contrast so no renal damage, but gives high radiation dose. KUBXR may show radiopaque stones.
Why is an ultrasound not used in the investigation of renal/ureteric stones?
Shows kidney stones well ish but poor at visualising ureteric stones.
Useful in pregnant and younger recurrent stone formers (no radiation risk).
How would you initially treat renal/ureteric stones?
- strong analgesic to relieve renal colic e.g. IV 75mg diclofenac
- antiemetic to prev vomiting
-most small ureteric stones (≤5mm) will pass spontaneously
How would you treat renal/ureteric stones if infection is present?
Antibiotics e.g. IV cefuroxime or IV gentamicin.
To prevent pyonephrosis
