Renal colic & urolithiasis

Renal colic & urolithiasis
Lilly Jenkins

Outline Epidemiology of urolithiasis
Stone pathogenesis : latest evidence contemporary risk factors Clinical presentation including renal colic Management : acute stone prevention Challenging cases in stone disease

Epidemiology Annual incidence 0.2% (US); 0.13% (Aust)
Prevalence 7% males, 3% females Risk of stone formation M : F = 3-4 : 1 (higher [Ucit] in women) Peak age yo Recurrence rate 10% at 1 yr (without Rx) 35% in 5 yrs 50% in 10 yrs Significant impact on QoL

Increasing stone incidence in Australia
Lee & Bariol, Epidemiology of Stone Disease in Australia, 2011

Evolution of stone management in Australia: increasing rate of intervention
Proportional comparison of stone treatment modalities for renal colic presentations between 2000–1 and 2007–8. © This slide is made available for non-commercial use only. Please note that permission may be required for re-use of images in which the copyright is owned by a third party. Evolution of stone management in Australia, Lee & Bariol, BJU International pages 29-33, 15 NOV 2011 DOI: /j X x

Evolution of stone management in Australia: less invasive but more frequent
Number of procedures claimed under Medicare Australia for different stone treatment modalities between 1995 and 2010. © This slide is made available for non-commercial use only. Please note that permission may be required for re-use of images in which the copyright is owned by a third party. BJU International pages 29-33, 15 NOV 2011 DOI: /j X x

Why has treatment rate outstripped incidence of stone presentations?
1. Increased rate of detection of asymptomatic stones: greater prevalence better imaging 2. Lower intervention threshold: opportunistic treatment during intervention for symptomatic stones 3. Loss of efficiency with less invasive Rx

Worldwide evidence Increasing incidence and prevalence, more pronounced in industrialized countries ? Lifestyle & dietary factors ? Better medical access – detection Renal stone formation & predominant stone composition are age & gender dependent Correlation b/w body wt & Uca excretion DM independent risk factor for stone development (Taylor & Curhan, AmJKid 2006) Male preponderance for all stone types except struvite Lower incidence struvite, uric acid incidence stable or same

Contemporary factors influencing stone formation
Dietary factors High protein and salt intake  risk of Ca stones High purine diets lower UpH and cause hyperuricosuria Vit B6 deficiency results in ^ formation and excretion of oxalate Low dietary calcium increases oxalate absorption Dehydration - excessive fluid loss, inadequate fluid intake Drugs - Ca supplements, indinavir Geographical factors Higher incidence during summer months & in tropical countries – effect of global warming on US “stone belt” shifting north (est cost $1 bn US by 2050) ? Mechanism -  urinary concentration & acidity or  Vit D production and Ca absorption.

Composition of renal stones
STONE TYPE Frequency (%) Calcium oxalate Calcium phosphate Mixed Ca ox and phos Struvite Uric acid Cystine Other (xanthine, drug metabolism) + noncrystalline ‘matrix’ makes up % Extensive investigations characterized matrix as a derivative of several of the mucoproteins of urine and serum; thought to play some role in stone pathogenesis

“Doctor, how / why did my stone form?”
Structural / anatomical problems Stone formation varies with stone type Exceeding supersaturation: uric acid & cystine Bacterial metabolism: struvite Calcium stones – most common but least understood

Calyceal diverticulum

Medullary sponge kidney
Medullary sponge kidney. A, Abdominal radiograph demonstrating calcifications diffusely scattered through the kidney. B, On an intravenous urogram the calcifications are seen to be engulfed by the excreted contrast within the dilated collecting ducts, which are more spherical in this case rather than tubular (as in Figs and 61-42).

“Doctor, how / why did my stone form?”
Structural / anatomical problems Stone formation varies with stone type Exceeding supersaturation: uric acid & cystine Bacterial metabolism: struvite Calcium stones – most common but least understood

Calcium stones: biochemical factors
Hypercalciuria Absorptive (intestinal) Renal leak Resorptive Hypercalcaemic Hypocitraturia Hyperuricosuria Hyperoxaluria

Factors influencing stone formation: Genetics
Idiopathic hypercalciuria -AD trait Cystinuria - AR, chr 2 Primary hyperoxaluria (type I and II) - AR Lesch - Nyhan syn (hyperuricaemia) - X-linked Others: familial RTA, Ehlers-Danlos syn, Marfan’s syn, Wilson’s disease Several disorders that cause renal stones are hereditary. Familial renal tubular acidosis (RTA) is associated with nephrolithiasis and nephrocalcinosis in almost 70% of patients (Dretler et al, 1969). Cystinuria is a homozygous recessive disease, and the genes that cause it have been cloned. Similarly, xanthinuria and dihydroxyadeninuria are rare hereditary disorders that cause renal stones

Family History 25% of patients with kidney stones have a family history of kidney stones (Curhan et al, 1997). Genetic studies performed by Resnick (1968) and McGeown (1960) concluded that urolithiasis may be the result of a polygenic defect with partial penetrance. White (1969) noted that urinary calcium excretion was significantly higher in spouses of patients who were stone formers than in spouses of persons who did not form stones ? household diet as well as familial tendencies must be considered in theories of etiology of urinary lithiasis

Pathogenesis & physicochemical properties
Factors influencing stone formation Genetics Environmental Physical and biochemical parameters Aetiological factors of specific stone types

Physical & biochemical parameters
Supersaturation - this depends on solute concentration, ionic strength, complexion, urine volume and pH. Crystal inhibitors: GAGs, Tamm-Horsfall protein, uropontin, citrate, pyrophosphate, magnesium Epitaxy - heterogeneous nucleation, ? nanobacteria Randall’s plaques - suburothelial papillary plaques resulting from interaction between renal epithelial cells and salt crystal; the crystals aggregate into large clumps which occlude the tubular lumen and erode toward the papillary surface to form a nidus for further stone growth. Anatomic abnormalities - reduced urine output and stasis predisposes to crystal retention in horseshoe kidney, calyceal / bladder diverticula, obstructive disorders and MSK. The central event in stone formation is supersaturation. I won’t go into the details of solubility products and so on, but a few facts are worth remembering: 1. Temperature and pH are always specified for any crystallization process 2. Urine is not water. urine is a much more complex solution than water. In urine, when the concentration of a substance reaches the point at which saturation would occur in water, crystallization does not occur as expected. Urine has the ability to hold more solute in solution than does pure water. Although all elements and molecules in urine are suspended in water, the mixture of many electrically active ions in urine causes interactions that change the solubility of their elements. In addition, many organic molecules, such as urea, uric acid, citrate, and complex mucoproteins of urine, affect the solubility of other substances. Similarly, the primary event in crystalization differs in water, a pure substance, and urine. The process by which nuclei form in pure solutions is called homogeneous nucleation. These nuclei form the earliest crystal structure that will not dissolve and have the form of a lattice that is characteristic of that crystal. In urine, however, crystal nuclei usually form on existing surfaces (heterogeneous nucleation). Epithelial cells, cell debris, urinary casts, other crystals, and red blood cells can all act as nuclei for crystallisation. Stones then grow on these preformed nuclei. The next important concept in the genesis of urinary calculi is that of aggregation. This is the process by which Crystal nuclei aggregate into large clumps which occlude the tubular lumen . The combination of growth and aggregation is the most popular explanation for stone formation today. Interference with crystal growth and aggregation is a possible therapeutic strategy for the prevention of recurrent stone disease, and the mechanism of action of several well known stone inhibitors (eg citrate, Mg, proteins) . If a crystal mass becomes lodged in the renal papilla or tubule, it is no longer able to move through the system. If a crystal is retained in the kidney, growth can occur for long periods of time whenever urinary supersaturation or aggregation of new crystals occurs. Many kidney stones have a layered structure, suggesting intermittent growth during periods of supersaturation. Urine does not need to be continuously supersaturated for crystals to form or grow: Intermittent supersaturation, as is seen during periods of dehydration or after meals, is sufficient. Urinary supersaturation alone cannot explain the formation of urinary stones. Urine contains substances that alter or modify crystal formatio, divided into inhibitors, complexors, and promoters. Inhibitors include low-molecular-weight compounds, such as citrate and pyrophosphate, and larger molecules, such as glycosaminoglycans, nephrocalcin, and Tamm-Horsfall protein. Finally, Anatomic abnormalities, such as medullary sponge kidney or ureteropelvic junction obstruction, or increased "stickiness" of the tubular epithelium can predispose to increased crystal retention and give rise to stone formation.

Pathogenesis & physicochemical properties
Factors influencing stone formation Genetics Environmental Physical and biochemical parameters Aetiological factors of specific stone types

Aetiological factors for Calcium stones
Hypercalciuria Absorptive: intestinal hyperabsorption with  Ca excretion due to filtered load and tubular reabsorption (due to PTH suppression); excessive renal Ca loss compensates for  absorption so serum Ca is normal. 2 types: Type I (AH-I) is severe Type II (AH-II) is mild - moderate form Renal (“renal leak”): primary anomaly is impaired renal tubular reabsorption, resulting in  PTH which stimulates Ca mobilisation form bone and gut absorption (via action of 1,25 DHD), further  filtered load causes significant hypercalciuria Resorptive: primary hyperparathyroidism stimulates excessive bone resorption and intestinal absorption Hypercalcaemia assoc with malignancy etc Hypercalcaemia causes: hyperparathyroidism cancers (lung, breast, RCC, head and neck, multiple myeloma), immobilisation, Pagets,, hypervitaminosis D, milk-alkali syn

Hypocitraturia: Common Citrate forms a soluble salt with Ca and inhibits the formation of Ca ox or phosphate crystals. Acidosis reduces Ucit by enhancing its tubular reabsorption and metabolism to bicarbonate. Causes: chronic diarrhoeal syn (assoc with enteric hyperoxaluria) distal (type I) RTA high salt/protein diet Hypokalaemia UTI (bacterial degradation of citrate) idiopathic Hypocitraturia - seen as sole abnormality in 5% of ptt with stones, and in 50% of ptt who have other metabolic disturbances

Hyperuricosuria: urate initiates ca ox stone formation by direct induction of heterogeneous nucleation or by adsorption of macromolecular inhibitors Hyperoxaluria: 3 main forms Dietary: high dietary content of oxalate or Vit C, or low calcium diet, may increase Uox to mg/d Enteric: bowel disturbance (IBD, short gut, J-I bypass) increases oxalate absorption due to (1) increased permeability due to action of bile salts and fa’s on mucosa, and (2) fat malabsorption increases Ca saponification and limits the calcium “pool’ available to complex with oxalate in the gut lumen (which is not absorbed). Primary: rare, types I and II, inherited enzymatic disturbances in oxalate biosynthesis Hyperoxaluria - usually due to intestinal hyperabsorption. This may be dietary.(NB Vit C is a substrate of oxalate). However the major cause is ileal disease or “enteric hyperox”.

Medullary nephrocalcinosis in a patient with renal tubular acidosis
Medullary nephrocalcinosis in a patient with renal tubular acidosis. Note the diffuse calcifications in both kidneys with the clusters of calcifications corresponding to the shape of the medullary pyramids.

Uric acid calculus. The stone was nonopaque on an abdominal radiograph
Uric acid calculus. The stone was nonopaque on an abdominal radiograph. A, The intravenous urogram can be misinterpreted as being normal, but a subtle filling defect can be seen in the renal pelvis (arrows). B, A retrograde pyelogram demonstrates to better advantage a heterogeneous nonobstructing calculus. C, A computed tomographic scan demonstrates that the calculus is of high attenuation.

Clinical manifestations
Asymptomatic - incidental discovery during unrelated Ix. Pain - mild ache Renal colic occurs when stones produce obstruction severe, sudden onset, intensifies over min Assoc nausea & vomiting Can’t sit still or get comfortable

Renal colic Sites of obstruction:
Calyx / infundibulum PUJ Pelvic brim, arching over iliac vessels Posterior pelvis (females) under broad lig / pelvic vv Above intramural ureter / VUJ - most common Pain distribution may vary with site of obstruction Irritative LUTS commonly associated with distal stones Pain for renal / prox ureteric stones : flank only; more distally tends to radiate into ipsilateral groin / testicle / labia

Assessment History: ? underlying cause for stones
Gout, FHx, IBD, hypercalcaemia Examination: fever, sepsis, tenderness MSU: pH - low: Urate, Ca ox high: Ca phos infection Bloods: WCC often raised, >15 ? Infection UEC, Ca, Urate

Investigation Radiology FBC UEC Urinalysis / microscopy / culture
Delayed - stone analysis serum Ca / UA / PTH 24 hr urine We’ll deal primarily with radiological Ix today, discuss metabolic Ix following acute Mx if time.

Radiological investigation
Options: KUB IVU Renal U/S Non-contrast helical CT Consider what you need to know: Obstruction Radio - opaque / lucent Site, number and size of stone(s), ie likelihood of spontaneous passage

KUB Quick, inexpensive and easily obtainable
Variable sensitivity % Useful adjunct to CT as a method of predicting stone composition – radiolucency = uric acid ? Dissolution Rx Useful for follow up KUB unless concerns about obstruction or stone lucency; then US or low dose NCCT 1-2% of cancers in US may be attributed to CT radiation sensitivity range - depends which paper you read; 92% of stones are at least partially radiopaque but doesn’t necessarily translate to visibilty - compete with no of factors include quality of the film, overlying bowel gas and faeces, underlying bony structures; most useful if read alongside CT or IVU, or as a progress film in someone with known , visible, radiopaque stones. A few ways to improve your yield with a KUB

Approach to the non-diagnostic KUB 1. Compare with previous XR
Use of previous films for evaluation of a distal ureteral stone in the presence of phleboliths. A, This film, obtained in a patient with acute left flank pain, appears to show a line of calcifications with a typical phlebolithic appearance (round with a central lucency) in the left anatomical pelvis. B, Review of a film obtained 6 months earlier shows that the calcification between the most proximal two phleboliths was not present (arrow in A). C, A film obtained 2 hours after injection of contrast material for intravenous urography shows columnization of contrast material to the stone in the left anatomical pelvis (arrow). The stone has migrated slightly more inferiorly than in A.

Obscuration of a large stone by the sacrum
Obscuration of a large stone by the sacrum. A, A preliminary film of the abdomen in a patient with acute onset of left flank pain was initially interpreted as negative for evidence of a radiopaque calculus. B, A slight left posterior oblique film suggests the presence of a faintly radiopaque calculus projected over the left sacral ala (arrow). C, Fluoroscopy with a steeper degree of obliquity improves the delineation of a 6-mm stone projected over the flat bone of the ilium. D, A film obtained 45 minutes into the intravenous urography sequence documents left hydroureteronephrosis to the level of the stone. E, A film obtained 48 hours later shows distal migration of the stone, which is now quite evident within the left anatomical pelvis. 2. Oblique views

Intravenous pyelogram
Variable quality Functional study Radiation dose less than CT Good anatomical detail for planning appropriate treatment Gallagher and Tolley AD: still a role for the IVU in stone management? Curr Opin Urology 2000

Typical intravenous urography (IVU) sequence in a patient with acute ureteral obstruction. A, A tomogram obtained 1 minute after contrast material injection for evaluation of acute left flank pain demonstrates approximately equivalent nephrographic effects, with delay in opacification of the collecting system on the left. B, An IVU film obtained at 15 minutes shows the development of a dense nephrogram on the left and a normal appearance of the collecting system on the right. Note the acute angle of the calyceal fornices in the normal collecting system. Continued C, A film obtained 24 hours after injection of contrast material demonstrates persistence of the nephrogram and mild dilatation of the intrarenal collecting system on the left. Note the rounded appearance of the calyceal fornices on the left when compared with those on the right side in B. The ureter is mildly dilated and shows columnization of contrast material to the level of a small stone in the distal part of the ureter (arrow). D, Columnization of contrast material in the ureter to the stone (arrow) is better appreciated on this left posterior oblique film obtained at the same time as C. Note also the appearance of the intrarenal collecting system.

Renal Ultrasound Procedure of choice for pregnant females
Assess for other causes of acute pain Not a functional study Hydronephrosis  Obstruction

Renal ultrasound Ultrasound demonstration of renal calculi. A, Densely echogenic calculi are present in the renal pelvis and lower-pole collecting system (arrows), with marked acoustical shadowing distal to the calculi (arrowheads). B, A scan at another level in the same patient shows upper-pole hydronephrosis (cross-marks) caused by an echogenic calculus within the upper-pole infundibulum (arrow). Acoustical shadowing is again well demonstrated.

Non-contrast helical CT Abd/Pelvis
Fast, highly sensitive and specific > 99% Strictly speaking is not a functional study, but can infer obstruction by indirect signs ie perinephric stranding, urinoma Can use in patients with contrast allergy Greater ability to detect alternative pathology Good anatomical detail with coronal reconstruction CT for prediction of stone composition CT densitometry: stone > 1000 HU more likely to fail SWL Stone size, position & skin-to-stone distance also assessable on NCCT and determine outcome Smith et al. Helical CT in diagnosis of urinary tract stones: Epidemiology, origin, pathophysiology, diagnosis and management. Radiol Clin N Amer 1999. Personal bias towards CT in the Ix of acute renal colic, but must admit IVU does facilitate treatment planning in particular for SWL.

Non-contrast helical CT
Right renal and ureteral calculi. Transaxial images through the kidney (A) and proximal right ureter (B) reveal two calculi associated with proximal right hydroureter and hydronephrosis. The "rim sign" is seen surrounding the right ureteral calculus in B, indicated by the presence of a thickened ureteral wall around the stone (arrow). This finding can help identify calcifications as ureteral calculi rather than as phleboliths.

Beware other diagnoses
Obstructing blood clot shown by non-contrast-enhanced computed tomography in a 70-year-old woman with gross hematuria and left flank pain. A, Left pyelectasis. B, High-attenuation clot (arrow) in the proximal segment of the left ureter. A subsequent intravenous urogram, retrograde ureteropyelogram, and nephroureteroscopy revealed no cause for the bleeding.

Management of stone disease
1. Acute - analgesia: NSAIDs, narcotic - observation - drainage 2. Definitive stone management if required - ureteroscopy - SWL - PCNL 3. Stone prevention

Management 1. Analgesia - oral, PR, parenteral - NSAIDs, narcotics
2. ?? iv fluids - if dry 3. Determine if renal unit is - obstructed - infected -> URGENT DRAINAGE 4. Other criteria for admission - ongoing pain, solitary kidney, renal impairment, pregnant 5. Rx: Conservative or Definitive if required -URS, SWL 6. Prevention – investigation of causes of urolithiasis, lifestyle modification, medication NSAIDs work by reducing prostacyclin-induced ureteric contractility; have been shown to reduce intrapelvic pressure and more recently (last WCE) ureteric urodynamics post URS diclofenac reduced ureteric peristalsis Another agent being Ix is desmopressin for Rx of acute renal colic

Renal colic – summary NCCT + KUB
KUB guides treatment planning & assists follow up of the stone Radiolucency on plain KUB is a surrogate indicator of stone composition Fever, tenderness ? sepsis FBC UEC

Treatment options Conservative: Drainage: Definitive
Consider chances of spontaneous passage - > 6 mm : 10% 4 - 6 mm : 50% < 4 mm: 90% Role of medical expulsive therapy - tamsulosin Drainage: Nephrostomy Stent Definitive Ureteroscopy SWL PCNL Laparoscopic or open surgery Must also consider other issues including patient’s preference, comorbidities and which modality is likely to render pt SF with the least fuss. URS and SWL to be covered next week.

Urolithiasis update 2009 CT for prediction of stone composition
CT densitometry: stone > 1000 HU more likely to fail SWL Stone size, position & skin-to-stone distance also assessable on NCCT and determine outcome Postop follow up KUB unless concerns about obstruction or stone lucency; then US or low dose NCCT 1-2% of cancers in US may be attributed to CT radiation

Spontaneous passage < 4mm : 90% 4 - 6 mm : 50% > 6 mm : 10%

If the rock is too large to pass, there are a number of Rx options available…

Ureteroscopy

Ureteroscopy Choice of energy source or removal
Technological advances in telescopes & paraphernalia

Ureteroscopes Innovations: Smaller size – primary treatment
Range of active deflection Digital flexible ureteroscope

Laser lithotripsy Ho:YAG – solid-state laser, 2100nm wavelength, pulsed Photothermal & photodynamic capacity: thermal fragmentation most efficient Pros: short tissue penetration due to water absorption(0.5 –1 mm), diverse applications incl stricture incision & tumour ablation, small fibers (0.2 – 0.6 mm) Cons: long pulse width (= lower pulse energy), ureteric injury Remains the best laser for stone disease in 2012

LASERTRIPSY REQUIREMENTS
Ureteroscope – rigid or flexible Holimium laser II, Radiographer Theatre team / Laser safety officer GA – minimal respiratory excursion Irrigation Paraphernalia Wires baskets

SWL Requirements: Shock wave generator Coupling mechanism Localisation
Image intensifier US

Percutaneous nephrolithotomy
Principles: Access Removal Drainage Combined Rx

PCNL innovations Swiss lithoclast master Flexible nephroscopes
Tubeless PCNL

Management of recurrent stone formers
General Fluids - how much ?? Lemon juice - boosts urinary citrate levels Specific Dietary advice - reduced protein, oxalate, NOT calcium Hyperuricosuria - Allopurinol, urinary alkalinisation Hypercalciuria - chlorthalidone

AVOID… Cheese - hardness proportional to Ca content
Moderate not restricted Ca diet so don’t increase oxalate reabsorption

ENCOURAGE….

Stone prevention: Investigation
Who do we investigate? Indications: recurrent stone former nephrolithiasis family history children solitary kidney systemic disease

Stone prevention: Investigation
How do we investigate? Includes: Stone analysis Serum Ca, PTH, Uric acid 24 hr urine : volume, pH Ca, Ox, Ph, UA, Cystine Magnesium, Citrate

Natural Prevention Dietary factors
Fluids: 1996 RCT showed 5yr stone recurrence rate 12%(high uo) vs 27% (low vol uo) Lemonade / OJ increase urinary citrate Animal protein (meat, chicken, fish) increases urinary ca, UA and phosphate. Salt increases ca & UA excretion. Restrict < 6g/day.

Natural Prevention Dietary factors
Fruit & vegetables: mixed results. Recommend standard daily intake (2+5), avoiding oxalate-rich foods (spinach, rhubarb, tomatoes, strawberries, rhubarb, beets, nuts, chocolate, tea). Dairy products: low calcium intake increases stone formation due to absorptive hyperoxaluria, therefore do not restrict

Specific measures Dissolution therapy (uric acid stones)
hydration pH manipulation – potassium citrate / sodibic Allopurinol if hyperuricosuric Hypercalciuria - Thiazides Cystinuria – fluids, low protein, alkaline urine (Uro-cit-K); binders – thiola, penicillamine

Urolithiasis: summary
Prevalent; M>F High recurrence rate: 50% within 10 yrs Definite role for investigation and prevention Use dietary measures initially More information? kidneystones.net.au

CHALLENGING CASES 1. Duplex ureter

2. Encrusted stent

3. Post SWL - Steinstrasse

4. Calyceal diverticulum

5. Medullary sponge kidney / multiple stones
Medullary sponge kidney. A, Abdominal radiograph demonstrating calcifications diffusely scattered through the kidney. B, On an intravenous urogram the calcifications are seen to be engulfed by the excreted contrast within the dilated collecting ducts, which are more spherical in this case rather than tubular (as in Figs and 61-42).

Medullary nephrocalcinosis in a patient with renal tubular acidosis
Medullary nephrocalcinosis in a patient with renal tubular acidosis. Note the diffuse calcifications in both kidneys with the clusters of calcifications corresponding to the shape of the medullary pyramids.

6. Stone in ureterocele / ureteric strictures
Stone within an orthotopic ureterocele. A, Plain film. Spiculated calculus is in the path of the right ureter. B, Intravenous urogram, 5 minutes, demonstrating incomplete duplication of the right ureter with a junction several centimeters above the bladder. An orthotopic ureterocele with a typical halo is present. The stone is hidden by contrast within the ureterocele. No hydroureretonephrosis was observed.

7. Horseshoe kidneys Horseshoe kidney

8. Pelvic kidney, transplant kidney, urinary diversion

9. Partial staghorn

Renal colic & urolithiasis

Similar presentations

Presentation on theme: "Renal colic & urolithiasis"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Renal colic & urolithiasis

Similar presentations

Presentation on theme: "Renal colic & urolithiasis"— Presentation transcript:

Similar presentations

About project

Feedback