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MSC: Disease of major orgns > Renal Stone Disease > Flashcards

Renal Stone Disease Flashcards

1
Q

Where can stones be located?

A

Urolithiasis: Refers to stone formation anywhere in the urinary

Stones can be located anywhere in the urinary tract

  • Kidney - Nephrolithiasis
  • Ureter - Ureterolithiasis
  • Bladder - Cystolithiasis
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2
Q

How do stones form?

A
  • Urine contains a variety of mineral ions (salts). Derived from diet / metabolism
  • The mineral ions in the urine can interact to form an insoluble complex (crystal) – Crystal Nidus
  • Multiple crystals stick together forming aggregates
  • Organic material can form between the crystals, forming an organic matrix: Proteins, Blood, Cell debris
  • Eventually a hard mass forms (stone)
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3
Q

What are common urinary stones?

A
  • Calcium Oxalate
  • Calcium phosphate
  • Struvite - Magnesium, Ammonia, Phosphate
  • Urate
  • Cystine
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4
Q

What are risk factors for stone formation?

A

Low urine volume

  • Dehydration, low fluid intake

Urine pH

  • Affects solubility of stone forming minerals

UTIs (Urinary tract infections)

  • Increase concentration of urine ammonia
  • Makes urine alkali, allowing calcium phosphate to crystallise more readily

Increased concentration of stone forming mineral ions in the urine e.g. oxalate, calcium, urate

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5
Q

What causes Hyperoxaluria?

A

Excess Dietary Oxalate

  • Chocolate, Tea, Rhubarb, Strawberries, Blackberries, Beetroot, Spinach

Reduced dietary Calcium

  • Results in increased oxalate absorption

Short bowel syndrome / fat malabsorption E.g. Crohn’s disease /pancreatic insufficiency

  • Increased fatty acids in intestinal lumen (malabsorption). The fatty acids combine with calcium. Increased concentration of free oxalates available for absorption

Primary hyperoxaluria (rare)

  • An increased synthesis of oxalate and excess oxalate excreted in the urine. It is caused by an enzyme deficiency leading to decreased breakdown glyoxylate.
  • Glyoxylate instead is converted to oxalate
  • Usually presents in childhood but can also present in adulthood

Idiopathic

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6
Q

What are causes of Hypercalcuria?

A

With Hypercalcaemia

  • Primary Hyperparathyroidism
  • Sarcoidosis
  • Vitamin D excess
  • Malignancy

With Normocalcaemia

  • Renal tubular acidosis
  • High sodium intake*
  • Prolonged immobilisation
  • Absorptive hypercalciuria**
  • Renal hypercalciuria
  • Increased bone turnover
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7
Q

What are causes of Hyperuraturia?

A
  • May be a result of dietary excess of purine rich foods e.g. Fish, Game, mutton, beef, pork, poultry
  • Tumour lysis syndrome
  • Gout
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8
Q

How is crystallisation inhibited?

A

Citrate and magnesium - inhibit formation of calcium salts (calcium oxalate)

  • Citrate forms soluble complexes with calcium
  • Magnesium forms soluble complexes with oxalate
  • Individuals with lower concentrations of citrate and magnesium are more likely to form stones than those with normal concentrations
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9
Q

What are cuases of Low citrate and magnesium in urine?

A

Hypocitraturia

  • Idiopathic
  • Renal tubular acidosis type 1
  • Hypokalaemia
  • Chronic diarrhoea
  • Antibiotics
  • Excess of animal protein
  • Diuretics such as thiazides

Hypomagnesuria

  • Poor nutritional intake
  • Chronic diarrhoea
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10
Q

How can Stones be prevented?

A

-Increase fluid intake

  • 2.5 – 3.0 L per day

-Dietary Advice. Can depend on type of stone

  • Balanced diet rich in vegetables
  • Normal calcium content: 1-1.2 g/day (don’t restrict intake)
  • Limited NaCl content: 3-5 g/day
  • Limited animal protein content: 0.8-1.0 g/kg/day

-Life style advice

  • Retain a normal BMI level & adequate physical activity

-Pharmacological intervention – depends on stone type

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11
Q

What is the treatment of existing stones?

A

Conservative approach – watch and wait!

  • Small kidney stones can usually pass by themselves and can be monitored by regular checks with ultrasound or X-ray

Medical expulsive therapy

  • Alpha blockers to inhibit muscle tone in the ureter, reduce intra-ureteral pressure and increase movement of fluid to help expel small distal stones

Extracorporeal shockwave lithotripsy (ESWL)

  • Uses high frequency sound waves from an external source (outside the body) to break up kidney stones into fragments and allow them to pass out through the urinary tract

Flexible Ureterorenoscopy

  • Uses a thin flexible telescope passed into the kidney via the ureter. Laser energy is used to break up kidney stones into fragments and the fragments collected using a ‘basket instrument’.

Percutaneous nephrolithtomy (PCNL)

  • Uses a ‘keyhole’ approach to pass a telescope into the kidney allowing the stone to be visualised
  • Using either laser or ultrasound energy the stone(s) are broken into fragments and removed through a small nephrostomy tube.

Open stone removal

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12
Q

What are their risk factors of Urate stones?

A

Hyperuraturia

  • Urine urate can be high or normal
  • (Urine urate can also be high in calcium oxalate stone formers)

Low urine pH (< 5.8) promotes urate crystallisation

  • Insulin resistance
  • Metabolic syndrome
  • Exercise-induced lactic acidosis
  • High animal protein intake
  • Increased base loss - diarrhoea

Hyperuricaemia

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13
Q

How are urate stones treated?

A

Reduce urate concentration in the urine

  • Limit purine rich foods: Fish, Game, mutton, beef, pork, poultry
  • Give allopurinol (if urine urate > 4.0 mmol/day): A higher dose is recommended if serum urate also high

Reduce acidity of the urine

  • Increase consumption of fruit and vegetables
  • Reduce intake of non-dairy animal protein
  • Give alkaline citrate or sodium bicarbonate to prevent further stones (if urine pH maintained at 6.2 – 6.8). Dissolves urate stones – chemolytholisis (if urine pH maintained at 6.5 – 7.2)
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14
Q

What are the types of Calcium Phosphate Stones?

A
  • Calcium monohydrogen phosphate dihydrate - Brushite
  • Calcium hydroxyl phosphate - Carbonate apatite

Can be present with calcium oxalate or struvite. It has a high risk of reoccurrence

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15
Q

What are causes/risk factors of calcium phosphate stones?

A

Brushite and Carbonate Apatite

  • Hypercalciuria
  • Hypocitraturia
  • High urine pH (6.5-6.8), (> 6.8)
  • Hyperphosphaturia (> 35 mmol/day) with Brushite
  • Urinary Tract Infections with Carbonate Apatite

​

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16
Q

What is the treatment of calcium phosphate stones?

A

Treat UTIs with antibiotics and ensure complete stone removal (Carbonate Apatite stones)

Treat underlying cause

  • Hyperparathyroidism – parathyroidectomy
  • Sarcoidosis - e.g. steroids
  • Renal tubular acidosis – alkaline citrate or sodium bicarbonate

Reduce urine calcium

  • Limit sodium intake
  • Give Thiazide diuretic

Reduce urine pH so less favorable conditions for calcium phosphate stone formation

  • Methionine to acidify urine - not commonly used due to risk of systemic acidosis.
  • Eat more vegetables and reduce animal protein
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17
Q

What is the structure of calcium oxalate stones?

A
  • Calcium Oxalate monohydrate – Whewellite
  • Calcium Oxalate Dihydrate – Weddellite

Also commonly combined with calcium phosphate, which are more likely to form at higher pH

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18
Q

How can formation of urine ph affect production of calcium oxalate?

A
  • Urine pH < 5.8 can promote co-crystallisation of uric acid and calcium oxalate
  • Uric acid excretion > 4 mmol/L/day can promote calcium oxalate stone formation.
19
Q

What are biochemical causes/risk factors of calcium oxalate?

A
  • Hypercalciuria
  • Hyperoxaluria
  • Hyperuricosuria
  • Hypomagnesuria
  • Hypocitraturia
20
Q

How is Calcium Oxalate treated?

A

-Hypercalcuria

  • Alkaline citrate or Sodium bicarbonate = Urine Ca 5-8 mmol/day
  • Thiazide = Urine 8 mmol/day

-Hyperoxaluria

  • Dietary reduction in oxalate and fat = >0.5 mmol/day (secondary)
  • Oral calcium with meals**not if hypercalciuria = >0.5 mmol/day (secondary)
  • Pyridoxine = > 1 mmol/day (primary)

-Hyperuricosuria

  • Alkaline citrate or sodium bicarbonate plus/or allopurinol = > 4mmol/day (enteric)
  • Alkaline citrate plus allopurinol for Hyperuricosuria and Hyperuricemia

-Hypocitraturia

  • Alkaline citrate or sodium bicarbonate
21
Q

What is the effect of Alkaline Citrate and Thiazide on Calcium Oxalate?

A

Thiazides

  • Increase renal tubular calcium absorption by inhibiting NaCl transporter which transports sodium into the renal tubule cell from the urine.
  • The reduction in cellular sodium stimulates reabsorption of Na from the blood in exchange for calcium which in turn causes absorption of calcium from the urine to balance cellular calcium so effectively reducing urine of calcium.

Alkaline citrate

  • Increases citrate in the urine which binds calcium but also increases pH which may reduce likelyhood of calcium oxalate monohydrate stone formation
22
Q

What are causes of Cystine Stone formation?

A

Cystinuria

  • Autosomal recessive disorder
  • Caused by mutation in an amino acid transporter in the proximal renal tubule
  • Means filtered cystine cannot be reabsorbed so builds up in the urine
  • Cystine is poorly soluble in urine
  • Can present at any age (commonest in second and third decade)
23
Q

Wat are risk factors for Cystine Stone formation?

A
  • Low urine volume
  • Acidic urine
24
Q

What is the treatment for Cystine Stones?

A
  • High fluid intake > 3.5 L / day. To maintain cysteine concentrations below saturation point
  • Limit sodium and protein intake
  • Maintain urine pH 7.5 – 8.5 (to improve cysteine solubility). Alkaline citrate and Sodium bicarbonate are used
  • Reduce urine cystine through Tiopronin
25
Q

What are causes of infected stones?

A
  • Magnesium ammonium phosphate – Struvite
  • Calcium hydroxyl phosphate - Carbonite apatite .
  • Ammonium urate (very rare)
26
Q

What is the formation of Infected Stones?

A
  • Can develop de-novo or on other stone types infected with urea-splitting bacteria. Urease-producing bacteria convert Urea → carbon dioxide + ammonia
  • This increases urinary ammonia to promote Struvite & Ammonium urate formation
  • This causes a raised pH which promotes Ammonium urate crystals (pH 6.5), carbonate apatite crystals (pH > 6.8) and struvite crystals (pH > 7.2)
27
Q

What are risk factors for Infected Stones?

A
  • Urinary tract infections
  • Gender: More common in women than men (increased risk of UTI in women)
  • Indwelling urinary catheter
  • Benign prostatic hyperplasia
  • Urinary tract obstruction
28
Q

What is the treatment for Infected stones?

A
  • Increase fluid intake
  • Complete surgical stone removal
  • Antibiotics (short or long term)
  • Urinary acidification using methionine or ammonium chloride (not common practice – can be dangerous)
29
Q

What are Xanthine stones and their treatment?

A
  • Xanthine oxidase deficiency (converts xanthine to uric acid) which causes Xanthinuria
  • Usually patient has low serum urate
  • Only treatment is reduction in dietary purines
30
Q

What are •2,8-dihydroxyadenine stones and their treatment?

A
  • Adenine phosphoribosyl transferase deficiency which causes high urinary 2,8-Dihydroxyadenine

Treatment

  • Can give allopurinol or febuxostat (under regular monitoring)
  • Reduction in dietary purines
31
Q

What are drugs that can affect the Urinary System?

A

Drugs that form stones

  • Allopurinol
  • Amoxicillin
  • Ampicillin

Drugs that impair urine composition

  • Ascorbic acid
  • Calcium
  • Vitamin D
  • Furosemide
  • Laxatives
32
Q

What are clinical presentations of Renal Stones in GP or A&E?

A
  • Can have no symptoms. If the stone stays in the kidney or found by chance on X-ray or scan
  • Urinary tract infections & haematuria
  • Burning pain on urination
  • Aching of the loin area
  • Ureteric colic (pain)
33
Q

What is a Ureteric Colic?

A
  • Severe pain occurring in spasms, usually in the loin area, radiating to the groin.
  • Nausea and vomiting
  • Occurs when a stone becomes impacted in the ureter
  • Renal tract obstruction → AKI
  • Complications can be sepsis - life-threatening
34
Q

What imaging is used to investigate stone?

A

Ultrasound

  • Initial imaging in patients presenting with renal colic
  • Identifies stones located various parts of the kidney

X-Ray

  • Stones can be classified according to appearance on plain X-ray
  • Appearance is based on mineral composition

Non-Contrast-enhanced Computed Tomography (NCCT)

  • Detects both radiolucent and radiopaque stones
  • Detects size and estimates ‘hardness’
35
Q

What does urinalysis show us?

A

Dipstick a mid stream urine to detect:

  • Blood → Haematuria
  • Approximate pH. Normal urine pH is 4.5 – 8.0. Ideally should be 5.5 – 6.5. < 5.8 (Can promote urate stones) and > 5.8 (suspicious of RTA / UTI)
  • Nitrates
  • Leukocytes
36
Q

What does Blood Analysis show?

A

-U&E

  • Exclude Acute Kidney Injury (AKI) caused by obstruction
  • Normal levels do not rule out obstruction

-Exclude common risk factors for urinary stones

  • Calcium and phosphate. High or high normal calcium - repeat with PTH
  • Urate

Full Blood count

-CRP

  • ? Infection

-A clotting screen

  • If percutaneous intervention is likely or planned.

-Blood cultures

  • If the patient is pyrexial >38°C, has signs of systemic inflammatory response syndrome (SIRS) or sepsis.
37
Q

What are the uses of stone composition analysis?

A
  • Basis for further diagnostic / management decisions
  • Detection of cystine, 2-8-Dihydroxyadenine or xanthine are pathognomonic for cystinuria and 2,8-dihydroxyadenine and xanthine oxidase deficiencies respectively
38
Q

Why isnt Stone compostion analysis always possible?

A
  • Stones not always collected – patients can be given sieves
  • Lithotripsy can result in little or no stone material
  • Stone does not always represent the initial metabolic derangement. Other material can accumulate on a pre-existing crystal nidus

If composition of stone is unknown. Use medical history, blood results and urinalysis with imaging to elucidate probable stone type

39
Q

What are further investigation?

A

Low Risk → No further investigation

  • Single stone
  • No history of stone formation
  • No biochemical abnormalities

High Risk → Metabolic Screen

  • Repeated stone episodes
  • Multiple stones at presentation
  • Family history of stones
  • Known diseases that predispose to stones
  • Gastro intestinal disease
  • Recurrent UTIs / infection stones
  • Stones containing brushite or urate
  • On drugs associated with stone formation
40
Q

What is a metabolic Screen?

A

Guidelines recommend two consecutive 24 hour urine collections while on patients normal diet and Ideally stone free for at least 20 day

  • Measure: Volume, pH, Calcium, Oxalate, Urate, Citrate, Magnesium, Sodium, Creatinine, Cystine

Collection bottle with:

  • Acid preservative: Calcium, citrate, oxalate
  • No preservatives: Urate, magnesium, creatinine.
41
Q

What are interpretations from metabolic screens?

A
  • Calcium: > 5.0 - hypercalciuria. Perform serum calcium, PTH, vitamin D, (ACE)
  • Oxalate: > 0.5 - suspicious of secondary hyperoxaluria (intestinal hyperabsorption of oxalate or extreme dietary oxalate intake). > 1.0 - suspicious of primary hyperoxaluria. Genetic testing conducted as a result
  • Urate: > 4.0 (women) > 5.0 (men) - hyperuraturia. Serum urate checked
  • Sodium: Normal range 40 -220 if serum sodium normal. Serum sodium checked
  • Citrate: < 2.5 - hypocitraturia
  • Magnesium: < 3.0 - hypomagnesuria
  • Phosphate: > 35 - hyperphosphaturia
  • Cystine: > 0.8 – cystinuria but can be normal in cysinuria – diagnosis is often by stone analysis. Urine and plasma amino acids checked and Nitroprusside test
42
Q

What are further test once the treatment has been initiated?

A
  • Random urine: Haematuria & Infection
  • 24 hour urine analysis
  • Blood analysis
  • Radiological investigations: Passage / location of stones & Formation of new stones

Initially at 8-12 weeks after pharmacological intervention. Then every 6 monthly to one yearly once normalised

43
Q

What are some radiopaque stone, radiopacity stones and radiolucent stones?

A

Radiopaque

  • Calcium oxalate
  • Calcium phosphate

Poor radiopacity

  • Struvite
  • Apatite

Radiolucent

  • Uric acid
  • Ammonium urate
  • Cystine
  • Xanthine
  • 2,8-Dihydroxyadenine
  • Drug-stones
44
Q
A

MSC: Disease of major orgns (23 decks)

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