Kidney Stone (Renal Calculus)

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Introduction

Renal calculi (kidney stones) are precipitates that form from urine due to a high concentration of that particular precipitate in the urine. The most common (85%) precipitate is calcium;  particularly calcium oxalate, about 10% are uric acid, and 5% due to other precipitates.

An example of a kidney stone
An example of a kidney stone
Kidney stones are likely to form where there is stasis, and they form more quickly once a nucleus has formed.
Kidney stones form in the kidney, where they are usually asymptomatic. Patients will typically present when the stone has dislodged from the kidney and become stuck in the ureter. The ureters gradually become narrower on their path from the kidney to the bladder. Stones can become stuck anywhere along this course, but the lower down the stone is at presentation, the more likely it is to pass without the need for surgical intervention.
  • For example, stones at the Vesicoureteric junction (VUJ) are more likely to pass than those in the mid-ureter
  • There may be a family history as genetic factors can lead to excretion of higher concentrations of the precipitates that form stones. There is a high chance of recurrence after a single episode as more stones are likely to form in the future – 50% at 5 years and 80% at 10 years
Patients classically present with severe colicky flank pain which may radiate to the groin. The pain is very severe – and patient may often writhe around on the bed or the floor in pain. The peristaltic action of the ureter squeezing on the stone is what causes the pain.
Large stones can cause a blockage (obstruction) of the ureter – causing hydroureter and hydronephrosis. In severe cases – this can impact renal function and be detected as elevated urea and creatinine and a low eGFR on blood tests. These patients typically require more urgent treatment. There is also the chance of a coexisting urinary tract infection or pyelonephritis.
Usually a CT scan (CT KUB) is performed to assess the location of the stone, and if there is any obstruction. Blood tests are performed to assess renal function (🇬🇧U+E / 🇦🇺UEC)
Management depends on the size of the stone, the location of the stone and any complications
  • Stones <5mm in size will typically pass without the need for surgical intervention. Medical management includes NSAIDs for analgesia (classically indomethacin 100mg PR or PO), and alpha-blockers (e.g. Tamsulosin 400mcg daily) to attempt to cause relaxation of the smooth muscle of the ureter to allow passage of the stone
    • There is also one small study that showed that in men – ejaculation can increase the rate of passing of stone without the need for surgical intervention- don’t forget to tell your patients to try this at home!
  • Stones larger than this, or with complicating factors are more likely to require surgical intervention. This typically involves two surgical procedures – the placing of a ureteric stent in the acute setting, and the removal of this stent several weeks later. Lithotripsy (breaking up of the stone – often via laser) may be performed at the same time as either or both of these procedure. This surgical procedure is usually performed via cystoscopy (an endoscopic procedure via the urethra).
  • Stones of <5mm will pass spontaneously in about 75% of cases
  • Stones of 5-10mm will pass spontaneously in about 50% of people
  • If the stone is <10mm (in the hospital where I work they use a cut-off of around 8mm) and has no complicating factors then patients may be discharged home with medical management – and booked for OP FU in a few weeks. If the stone hasn’t passed they are likely to be offered surgical intervention. In really lots of these patients represent to the emergency department before this time as they can’t tolerate the pain.

In the long-term – patients may be advised to make certain dietary changes to lower the amount of calcium oxalate int heir urine to reduce the risk of recurrence.

Epidemiology

  • More common in men
  • Occurs in about 1/1000 individuals
  • By Age 70, 12% of men and 5% of women will have been affected
  • More common in older age groups – as they take years to form

Aetiology

  • Is generally multifactorial. It is believed that about 50% of cases are due to a hereditary disorder – hypercalcuria which results in increased urinary concentrations of calcium, despite normal serum ca2+ concentrations.
  • Hyperparathyroidism is also known to increase the risk due to its effects on calcium metabolism.
  • Salt, sugar and animal protein can increase the risk of stones. Anything that’s brown / red that you eat increases the risk of stones (tea / coffee / coke / rhubarb / radishes / strawberries).
  • Low calcium diet is NOT useful as the body will counteract this by breaking down bone to raise calcium levels.
  • High risk of recurrence – 50% at 5 years and 80% at 10 years

Pathology

Stones tend to form in the kidney itself or in the renal pelvis. The problems occur when the stone passes down from the renal pelvis into the ureter, and get stuck. Many stones (usually those <5mm) will pass freely down into the bladder, and then leave the body in the urine, but larger stones (>5mm) can become stuck in the ureter. Common sites of obstruction are the:
  • Uretopelvic junction
  • Vesicoureteric junction (VUJ)
A phlebolith may mimic a stone. This is a calcification of a valve (vein) in the pelvis.
Stones more commonly form at the bottom of the kidney as a result of urinary stasis.

Presentation

Pain – a classical colicky loin pain. Patients often describe it as the worst pain they have ever felt! Patients will typically writhe around in pain and find it difficult to get comfortable. The ureters contract in a peristaltic manner, and move a ‘bolus’ of urine down from the pelvo-uteric junction (PUJ) down along the ureters. The pain felt in renal colic occurs every time the ureters contract and press onto the obstructing stone. The loin pain classically radiaties down and round (L1-L2 nerve routes). It may go to the vulva/clitoris in females, and the tip of the penis in males.
Nausea / Vomiting
Haematuria
Sepsis

  • Fever (above 38, you become impaired, above 40 you may hallucinate). You increase your temperature to reduce the effectiveness of bacterial enzymes.
  • Dysuria (burning pain on micturation)
  • Tachycardia
  • Decreased blood pressure – can lead to septic shock.
  • Gram-negative bacteria are particularly dangerous
A kidney stone with finger for scale. Painful little things!
A kidney stone with finger for scale. Painful little things!

Differential diagnosis

Investigations

Urinalysis – haematuria is common, but unless there is accompanying sepsis, urine will likely otherwise be normal.
AXR

  • About 85% of stones will be visible on plain AXR
  • Hilum of the kidney is about the level of L1.it moves with respiration (because it is retronperitoneal) On x-ray you can count up from L5 to L1 to check the level of a stone.

IVU – Intravenous Urogram

  • Good to demonstrate the presence of location of a stone, but IV contrast carries risks. CT is often preferred if available.

CT

  • CT KUB (Kidneys, Ureters, Bladder) is now usually the investigation of choice.
CT KUB showing the presence of multiple stones in the kidneys - but none in the ureters
CT KUB showing the presence of multiple stones in the kidneys – but none in the ureters

Management

Often conservative, especially if stone is less than 5mm.

Analgesia!

  • NSAIDs are useful as they aid with relaxation of ureteric smooth muscle. Diclofennac is usually the NSAID of choice as it is more potent than ibuprofen, and can be given PR, as many patients are nauseus / vomiting. Be wary in asthma.
  • Codeine/ morphine

Smooth muscle relaxants

Small smooth stones may pass themselves
Stone may be passed depending on where it is, and urinary flow (which may be reduced due to renal failure)
Mid-ureter – 60% chance of passing
Invasive management – if conservative is unsuccessful

  • Extracorporeal shock wave lithotripsy – using waves, break up the stone
  • Endoscopic – along natural tubes
  • Endoscopic percutaneous
  • Endoscopic – laparoscopic very rare
  • Open operation. Very rare
  • Impacted stones will need intervention – this is where the contractions of the ureters will not move the stone, and this irritates with mucosa and lead to oedema, which then makes the stone even harder to pass! This can lead to stricture.
  • Steinstrasse – ‘stone street’ this is a phenomenon that can occur after you have broken down all the stones with lithotripsy. The stones may all try to move down the ureter at once and become impacted, effectively forming one larger body again.

Uric acid stones – often do not show up on x-ray. They are common in gout, and can be treated with allopurinol.

You need to intervene if:
  • Pain
  • Sepsis
  • There is previous kidney damage, impaired renal function.
Good fluid intake is the best preventative measure for preventing stones.

Complications

  • Renal failure – any obstruction to the ureter will cause backflow and affect the GFR in the effected kidney.  However, permanent damage is unlikely to result from hydronephrosis unless the obstruction is present for weeks at a time.
  • Sepsis – is more common than renal failure, but still generally unlikely.

Secondary prevention

  • Thiazide diureticsare useful in those with hypercalcaemuria as they help to reduce calcium excretion.

References

  • Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
  • Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
  • Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
  • Urolithiasis – patient.info

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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