Introduction

Renal 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.

They are likely to form where there is stasis, and they form more quickly once a nucleus has formed.

Epidemiology

  • More common in men
  • Occur in about 1/1000 individuals
  • By Age 70, 12% of men and 5% of women will have been affected
  • More common in elderly 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.

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

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

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 diuretics – are useful in those with hypercalcaemuria as they help to reduce calcium excretion.

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