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Nephrolithiasis Eva Jančová
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Nephrolithiasis Renal and ureteral stones are a common problem in primary care practice Primary care physicians need to be alert to the possibility of nephrolithiasis and its consequences to decide upon a diagnostic approach, therapy, and refferal to a urologist or stone specialist
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Epidemiology The prevalence of renal calculi varies with the population studied The rate of nephrolihiasis increases with age (is higher in men compared to woman) whites compared to blacks Patients discharged from hospital with diagnosis of stones 1.8 per Incidence of stones in general practice 7 per General practice incidence of stones in males aged 45–60 years 21 per
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Etiology 85% of pts with n. form calcium stones
most of which are composed primary of calcium oxalate less often calcium phosphate The other main types include Uric acid Struvite (magnesium ammonium phosphate) Cystine stone The same pts may have more than one type of stone currently Calcium and uric acid
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Major Risk Factors for Calcium Stones
Low urine volume Hypercalciuria Hypocitraturia Hyperuricosuria Dietary factors Low fluid intake Type of fluid intake-soft drinks, apple or grapefruite juice High protein intake Low calcium intake History of prior calcium stones Hyperoxaluria (eg, enteric hyperoxaluria) Meddulary sponge disease Unexplained association with disorders-hypertension, vasectomy
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Other factors affect the risk of stone formation
History of prior calcium nephrolithiasis Family history of nephrolithiasis Inhanced of entetric oxalate absorption Urinary tract infection Medivations /indinavir, sulfadiazine,…)
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Clinical presentations of urinary stones
Urinary tract infections Acute (single or recurrent attack) Chronic Pyonephrosis Calculus anuria Strangury and interruption of urine stream Pain Ureteric colic Lumbar ache On micturition Haematuria Sterile pyuria Asymptomatic proteinuria Dysuria and increased urinary frequency
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Clinical manifestions
Patients may occasionally be diagnosed with asymtomatic nephrolithiasis The asymptomatic phase is more likely persist in those who have never had a clinical episode of renal colic
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Clinical manifestions-Symptoms
Patients occasionally present after already having passed gravel or a stone Uric acid stones are more likely present with gravel but they cal also produce acute obstruction
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Clinical manifestions
Symptoms are usually produced when stones pass from the renal pelvis into the ureter Pain is the most common symtom and varies from a mild and barely noticeable ache, to discomfort which is so intense that it requires hospitalization and parenteral medications
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Clinical manifestions-Pain
The pain typically waxes and wanes in severity, and develops in waves or paroxysms that are related to movement of the stone in the ureter and associated ureteral spasm Pain is thought to occur due to muscular contraction of the ureter in response to the stone
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Clinical manifestions-Pain
The site of obstruction determines the locaton of pain Upper ureteral or renal pelvic obstruction lead to flak pain or tenderness Lower ureteral obstruction causes pain that may radiate to the ipsilateral testicle or labia The location of the pain may change as the stone migrates
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Clinical manifestions-Pain
Variable location of pain can be misleading and occasionally mimics an acute abdomen or dissecting
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Clinical manifestions-Hematuria
Gross or microscopic hematuria occur in the majority of patients presenting with symptomatic nephrolithiasis Unilateral flank pain, hematuria, and a positivity plain of the abdomen are present in 90 percent of emergency room patients with a stone Absence of hematuria in the setting of acute flank pain does not exclude the presence of nephrolithiasis
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Clinical manifestions
Other symptoms Nausea Vommiting Dysuria Urgency Complicantions Persistent renal obstruction Sepsis
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Differential diagnosis
Ectopic pregnancy Aortic aneurysm Acute intestinal obstruction Renal carcinoma (bleeding within the kidney)
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Diagnosis The diagnosis of nephrolithiasis is initially suspected by clinical presentation Confirmatory radiologic tests include Abdominal plain film (KUB) Intravenous pyelography (IVP) Ultrasonography CT scan (including spiral CT) MRI
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Abdominal plain film (KUB)
Will identify radiopaque stones Calcium-containing stones Struvite stones Cystine stones
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Abdominal plain film (KUB)
Advantages Readily available Inxpensive Limited radiation Useful in acute setting Disadvantages Requies skilled radiologist to interpret Limited sensitivity and specificity
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Intravenous pyelography (IVP)
High sensitivity and specificity for detection of stones and provides data about the degree of obstruction
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Intravenous pyelography (IVP)
Advantages Useful in planning therapy and confirming diagnosis Long established history as gold standard Disadvantages Moderately expensive Intravenous contrast required Moderate x-ray exposure
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Ultrasonography Advantages Disadvantages Readily available
Roughly equivalent to IVP as a diagnostic test Improved sensitivity with use of color Doppler No radiation exposure Good for hydronephrosis Disadvantages Moderately expensive Poor performance with small stones Requires skilled technician and radiologist
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CT scan (including spiral CT)
Advantages Probably new gold standard Can distinguish radiolucent stones from blood and tumor Disadvantages Expensive Moderate x-ray exposure Not uniform available
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MRI Advantages Disadvantages
Great potential for localizing sight of stone in ureter Disadvantages Vera expensive Largely investigational so far except in certain centres
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Results of diagnostic imaging in patients presenting with renal colic
Sites of calcific lesions which may be confused with radio-opaque urinary stones: gallstones, costal cartilages, mesenteric lymph nodes, adrenals, pancreas, renal and splenic arteries, pelvic veins. The radiotranslucent stones uric acid, xanthine, oxipurinol, 2,8-dihydroxyadenine, orotic acid, and triamterine. Finely stippled nephrocalcinosis suggests long-standing hypercalcaemia Dense coarse nephrocalcinosis suggests primary hyperoxaluria or renal tubular acidosis.
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Results of diagnostic imaging in patients presenting with renal colic
Obstructive uropathy due to: Radio-opaque stone Radiotranslucent obstructive lesion (stones, crystals, sloughed papillae, clots, carcinoma) Generalized nephrocalcinosis Medullary sponge kidney Renal papillary necrosis (sloughed papilla) Cortical scars due to chronic pyelonephritis Renal carcinoma (cause of ‘clot colic’) Coincidental calcific lesion (e.g. tuberculosis, Randall’s plaques)
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Acute Therapy Pain control Hydration Urology consultation
Nonsteroidal antiinflammatory drugs (NSAIDs) Narcotics Hydration Urology consultation
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Acute Therapy Patients can be managed at home if they are able to take oral medications and fluids Hospitalization is required for those who cannot tolerate oral intake have very severe pain
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Acute Therapy Hospitalization is required for those who
cannot tolerate oral intake have very severe pain
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Urology consultation Urgent urologic consultation is warranted in patients with Urosepsis Acute renal failure Outpatient urology referral is indicated in patients Who fail to pass the stone after a trial of conservative management (usually two to four weeks) A stone more 5mm in diameter Uncontrolled pain
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Diagnosis and acute managment of suspected nephrolithiasis
Epidemiology Etiology Clinical manifestation Differential diagnosis Diagnosis Acute therapy Evaluation and subsequent treatment
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Evaluation and subsequent treatment
The patient shoud be evaluated for possible underlying causes of stone disease These include: Hypercalcemia Hypercalciuria Hyperuricosuria Hypocitraturia Hyperoxaluria
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Evaluation and subsequent treatment-Calcium stones
Composed purely or predominantly of calcium oxalate can occur in many differënt disordes Calcium phosphate stones are associated with the same risk factors as calcum oxalate stones. One exception- calcium phosphate stones are more typical of complete or incomplete distal renal acidosis
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Calcium stones Oxalate crystals
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Urinary risk factors for idiopathic calcium stones
Low volume, which increased the concentrations of the lithogenic factors Hypercalciuria, with or without hypercalcemia Hyperuricosuria, which in calcium oxalate-stone formers, is usually due to increased protein intake and therefore uric acid production Hypocitraturia, which can be marked in patients wih chronic metabolic acidosis Hyperoxaluria, which may be present in up to 40 percent of male and 15 percent of female stone formers Defects of macromolecular inhibitors
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Urinary risk factors for idiopathic calcium stones
Calcium stone formation is most often idiopathic, but can occur a number of other disorders.
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Underlying systemic or renal disorders in calcium stone disease
Primary hyperparathyroidism Medullary sponge kidney Distal renal tubular acidosis (complete or incomplete) Sarcoidosis (and other granulomatous diseases) Hyperoxaluria Enteric Primary
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Evaluation and subsequent treatment-Uric acid stones
Pure uric acid stones primary occur in patients in whom a persistently acid urine promotes uric acid precipitation In the absence of gout, uric acid stones may be seen other causes of chronic overproduction of uric acid or in chronic diarrheal states in which bicarbonate loss and volume depletion lead to a concentrated, acid urine
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Caused of Secondary due to increased Purine Biosynthesis and/or Urate Production
Inherited enzyme defects leading to purine overproduction Clinical disorders leading to purine and/or overproduction Myeloproliferative disorders Lymfoproliferative disorders Malignancies Hemolytic disorders Psoriasis Obesity Tissue hypoxia Down Syndrome Glycogen storage diseases (type III,V,VII)
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Caused of Secondary due to increased Purine Biosynthesis and/or Urate Production-continue
Drug-,diet, or toxin-induced purine and /or urate overproduction Ethanol Excessive dietary purine ingestion Pancreatic extract Fructose Vitamin B12 (pts with pernicious anemia) Nicotinic acid Cytotoxic drugs Warfarin
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Evaluation and subsequent treatment-Struvite stones
Struvite stones only form in pts with a chronic urinary tract infection due to a urease production organism such as Proteus or Klebsiella The stone may grow rapidly over a period of week to months and, if not, adequately treated, can develop into a staghorn or branched calculus involving the entire renal pelvis and calyces
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Evaluation and subsequent treatment-Cystine stones
Cystine stones developt in pts with cystinuria due to the insolubility of cystine in the urine The diagnosis of cystinuria is made from the family history, by identification of the pathognomonic hexagonal cystine crystal on urinalysis
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Cystine stones Typical hexagonal crystals of cystine under (a) non-polarized and (b) polarized light.
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Focused History All pts with a first stone should undergo a focused history to identify stone risk factors such as a family history of stone disease and certain dietary habits Low fluid intake (high concetration of lithogenic factors) High animal protein diet (which can lead to hypercalciuria, hyperuricosuria, hypocitraturia High salt diet (which increases urinary calcium excretion) Increased intake of oxalate-containing foods Vitamin D supplements
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Investigations in a Calcium Stone-former
Blood tests Serum calcium 2-3x Serum uric acid Serum bicarbonate Serum creatinine (electrolytes) PTH
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Investigations in a Calcium Stone-former
Urinalysis Urine microscopy and culture Urine pH 24-hour collections (2-3x) Volume pH creatinine calcium oxalate uric acid citrate (sodium) (urea)
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Methods for stone analysis
Wet chemical analysis (qualitative or quantitative) Optical crystallography X-ray diffraction Thermogravimetric analysis Scanning electron microscopy IR spectroscopy
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Evaluation and subsequent treatment
Subsequent therapy is based upon the type of stone and the biochemical abnormalities that are present Therapy to prevent new stone formation is required: All pts shoud increase fluid intake to above 2L/day, including drinking at night Pts with calcium stones can be treated with a thiazide diuretic and low sodium diet for hypercalciuria, allopurinol for hyperuricosuria, and potassium citrate for hypocitraturia
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Evaluation and subsequent treatment
Therapy to prevent new stone formation is required-continued: Pts wit uric acid stones can bez treated with potassium citrate to alkalinize the urine ao allopurinol Pts with cystine stones can be treated with high fluid intakem urinary alkalinizatin, and drugs such as penicillamine or captopril Treatment of struvite stones is difficult
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Causes of macroscopic nephrocalcinosis (cortical x medullary)
Chronic glomerulonephritis Acute cortical necrosis Chronic pyelonephritis Benign nodular subcapsular
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Nephrocalcinosis Cortical nephrocalcinosis (necropsy specimen)
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Causes of macroscopic nephrocalcinosis (cortical x medullary)
Oxalosis Distal renal tubular acidosis Acetazolamide Dent's disease Hypomagnesaemia-hypercalciuria syndrome Medullary sponge kidney Renal papillary necrosis Others (Williams' and Bartter's Medullary Autonomous hyperparathyroidis Milk alkali syndrome Hypervitaminosis D Sarcoidosis Idiopathic hypercalciuria MacGibbon–Lubinsky syndrome
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Nephrocalcinosis Medullary nephrocalcinosis in a 25-year-old man with familial distal renal tubular acidosis.
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Prognosis for overall renal function-continue
Best Idiopathic hypercalciuria Medullary sponge kidney Distal renal tubular acidosis Autonomous hyperparathyroidism and other rectifiable hypercalcaemias Papillary necrosis Dent’s disease/X-linked recessive nephrolithiasis Hypomagnesaemia–hypercalciuria (Michelis–Manz) syndrome Worst Primary hyperoxaluria, type 1
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Renal Neoplasms
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Renal Cell Carcinoma Primary renal neoplasms Secundary renal neoplasms
Transitionla cell carcinoma (6%) Oncocytomas Collecting duct tumors Rema sarcomas Nephroblastomas Secundary renal neoplasms Rarelly
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Clinical features Hematuria Abdominal or flan mann Scrotale varicocele
Vena cava involvement (ascies, hepatic dysfunction, pulmonary emboli) Systemic or paraneoplastic syndroms Fever Cachexia Amyloidosis Anemie Hepatic dysfunction Erythrocytosis and thromocytosis Hypercalcemia Polymyalgia-like syndrome
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