Siswoyo. Dep. KMB-Kritis PSIK UNEJ. Urolithiasis, kidney stones, renal stones, and renal calculi are used interchangeably to refer to the accretion of hard. Nephrolithiasis (K16) Final – Download as Powerpoint Presentation .ppt Documents Similar To Nephrolithiasis (K16) Final Askep Batu Ginjal-sis (2). pptx. Nephrolithiasis – Download as Powerpoint Presentation .ppt), PDF File .pdf), Text File .txt) or view presentation slides online. askep urolithiasis. uploaded by.
|Country:||Republic of Macedonia|
|Published (Last):||13 April 2010|
|PDF File Size:||8.9 Mb|
|ePub File Size:||9.45 Mb|
|Price:||Free* [*Free Regsitration Required]|
The pathogenetic mechanisms of kidney stone formation are complex and involve both metabolic and environmental risk factors.
Pencegahan Tonsilitis | Askep Tonsilitis | Pinterest | Medical, Sore throat and Clinic
Over the past decade, major advances have been made in the understanding of the pathogenesis, diagnosis, and treatment of kidney stone disease. Both ne;hrolithiasis and review articles were found via PubMed search reporting on pathophysiology, diagnosis, and management of kidney stones.
These resources were integrated with the authors’ knowledge of the field. Nephrolithiasis remains a major economic and health burden worldwide. Nephrolithiasis is considered a systemic disorder associated with chronic kidney disease, bone loss and fractures, increased risk of coronary artery disease, hypertension, type 2 diabetes mellitus, and the metabolic syndrome.
Further understanding of the pathophysiological link between nephrolithiasis and these systemic disorders is necessary for the development of new therapeutic options.
Acute and chronic kidney injury in nephrolithiasis
The increased prevalence of kidney stone disease is pandemic nephrrolithiasis. Nephrolithiasis has become increasingly recognized as a systemic disorder 3 that is associated with chronic kidney disease, nephrolithiasis-induced bone disease 4increased risk of coronary artery disease, hypertension, type 2 diabetes mellitus, and the metabolic syndrome MS 5.
The prevalence of nephrolithiasis in the United States has doubled over the past three decades. This increase has also askepp noted in most European countries and Southeast Asia 1.
Racial and ethnic differences are seen in kidney stone disease, primarily occurring in Caucasian males and least prevalent in young African-American females.
The prevalence in Asian and Hispanic ethnicities is intermediate 1.
The incidence of nephrolithiasis is highest in Caucasian males 2where the incidence of kidney stones rises after age 20, peaks between nepphrolithiasis and 60 yr of age at approximately 3 per per yearand then declines 8.
In females, the incidence rate is higher in the late 20s, decreases by age 50, and remains relatively constant thereafter 28.
The pathophysiological mechanisms for calcium kidney stone formation are complex and diverse and include low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH Table 1 Hypercalciuria is the most prevalent abnormality in calcium kidney stone formers.
InFlocks 13 initially described the link between hypercalciuria and nephrolithiasis. However, intestinal calcium hyperabsorption is the most common abnormality in this population Nevertheless, all the aforementioned physiological defects may coexist in individual patients, leading to decreased bone mineral density and bone fracture 4.
Hypercalciuria is a heterogeneous disorder in which intestinal calcium hyperabsorption may be dependent 2021 or independent 1922 — 25 of 1,dihydroxyvitamin D [1,25 OH 2 D]. Classically, hypercalciuria is classified into two different groups. In two studies, increased serum 1,25 OH 2 D concentration was reported in the majority of kidney stone formers with hypercalciuria 20 The underlying mechanism s of enhanced 1,25 OH 2 D production have yet to be elucidated.
However, in the majority of well-defined hypercalciuric stone formers, the main regulators of 1,25 OH 2 D production, namely serum PTH, phosphorus, and tubular maximum renal phosphorus reabsorption, were all at comparable levels to those of normal non-stone-forming subjects Few studies have suggested a link between renal tubular phosphorus abnormalities and serum 1,25 OH 2 D levels 20 Further supporting the role of 1,25 OH 2 D -mediated hypercalciuria, several studies have shown excessive urinary calcium excretion in normal subjects challenged with a large dose of 1,25 OH 2 D 20 However, a disagreement has arisen between the origin of hypercalciuria in which one study supports the intestinal origin 20 and the other suggests calcium mobilization from bone Despite reports of high circulating 1,25 OH 2 D in hypercalciuric stone formers 2021several studies have shown that hyperabsorption of calcium is independent of vitamin D, with over two thirds of idiopathic hypercalciuric patients exhibiting increased intestinal calcium absorption with normal prevailing serum 1,25 OH 2 D concentration 1922 — To probe this possibility, short-term administration of ketoconazole, an antimycotic agent known to reduce serum 1,25 OH 2 D, was shown to significantly lower serum 1,25 OH 2 D concentration without a significant alteration in intestinal calcium absorption in hypercalciuric subjects Similarly, treatment with thiazide, glucocorticoids, and phosphate was not shown to influence intestinal calcium absorption in this population, suggesting that calcitriol has a limited pathophysiological role in hypercalciuria 2530 Several studies have exhibited similar phenotypic characteristics in a model of hypercalciuric stone-forming rat GHS rat.
These studies demonstrated normal serum calcium and calcitriol concentrations, increased intestinal calcium absorption with the presence of CaP and CaOx stones 3233enhanced bone resorption, and diminished renal tubular calcium reabsorption 3234 In this rat model, an increased abundance of vitamin D receptor VDR was shown with normal circulating calcitriol levels and increased VDR protein in the intestine, kidney, and bone that was attributed to increased VDR half-life 34 These results support the notion that prolonged VDR half-life increases VDR tissue expression, resulting in hypercalciuria mediated via VDR-regulated genes controlling vitamin D-regulated calcium transport mechanisms The biological action of the VDR-1,25 OH 2 D complex was supported by increased expression of both 9- and kDa calbindin levels in the duodenum and renal cortical tissue of the GHS rat Renal leak hypercalciuria is a second, less common variety of hypercalciuria in which defective renal tubular calcium reabsorption is accompanied by enhanced PTH, calcitriol, and net intestinal calcium absorption Studies using a single dose of hydrochlorothiazide in both unselected and selected groups of calcium stone formers have linked defective renal calcium reabsorption to a proximal renal tubular defect 16 The most common prototype of resorptive hypercalciuria is primary hyperparathyroidism.
Hypercalciuria is perceived as a cause of kidney stones in this population. Nevertheless, the exact relationship between hypercalciuria and the risk of nephrolithiasis with primary hyperparathyroidism is not fully agreed upon 40 It has been disputed whether hypercalciuria originates from increased calcium mobilization from bone or reflects increased intestinal calcium absorption 4042 It is suggested that kidney stones are more prevalent in younger populations with primary hyperparathyroidism due to enhanced synthesis of 1,25 OH 2 D with intact kidney function, and consequent increased intestinal calcium absorption Bone disease may occur in older subjects due to their lower serum 1,25 OH 2 D levels and consequently diminished intestinal calcium absorption.
The pathophysiological mechanism underlying hyperuricosuria is attributed to a high purine diet However, in approximately one third of patients, endogenous uric acid UA overproduction prevails, and dietary restriction does not significantly alter urinary UA excretion The physicochemical basis involved in this process has not been well established.
Additionally, a retrospective population-based study in a large number of patients has not shown a relationship between urinary UA and CaOx stone formation The major determinant of urinary citrate excretion is acid-base balance Hypocitraturia commonly occurs with metabolic acidosis or acid loading mediated through up-regulation of proximal renal tubular reabsorption of citrate The main conditions include distal renal tubular acidosis dRTA 53carbonic anhydrase inhibitors 5455and normal bicarbonatemic states 56including incomplete dRTA 57thiazide treatment with hypokalemia 58primary aldosteronism 59high protein consumption 60excessive salt intake 61and converting enzyme inhibitors The physicochemical basis for the inhibitory role of citrate involves the formation of soluble complexes and reduction of urinary saturation with respect to calcium salts in addition to direct inhibition of CaOx crystallization processes Urinary oxalate and calcium are equally important in raising urinary CaOx supersaturation 5.
The underlying mechanisms of hyperoxaluria can be divided into: Subsequent investigation substantiated such a mutation; however, it remains unknown how changes in enzyme activity result in hyperoxaluria Recently, Oxalobacter formigenes in humans have been proposed to participate in intestinal oxalate metabolism Although a putative anion exchange transporter SLC26A6 has been shown to play a key role in intestinal oxalate absorption in mice, phenotypic and functional analysis has excluded a significant effect of identified variants in the corresponding human gene on oxalate excretion in humans 70 In enteric hyperoxaluria, the underlying mechanisms are purported to be increased permeability to oxalate with unabsorbed bile acid and fatty acids interacting with divalent cations in the lumen of the intestine, thereby raising intestinal luminal oxalate content and resulting in excessive urinary oxalate excretion In addition to hyperoxaluria, these disorders are associated with multiple other kidney stone risk factors including low urine volume, hypocitraturia, hypomagnesuria, and highly acidic urine.
With unduly acidic pH, urine becomes supersaturated with undissociated UA that participates in CaOx crystallization In clinical practice, conditions associated with CaP stone formation include dRTA, primary hyperparathyroidism, and use of carbonic anhydrase inhibitors 75 One suggested mechanism for the formation of calcium stones is increased urinary supersaturation of stone-forming salts, which leads to homogeneous nucleation in the lumen of the nephron, followed by crystal growth and consequent obstruction in the distal nephron 5.
However, over the past decade nephrolithiass has become apparent that CaOx stone formation differs histologically from that of CaP CaOx stones have been shown to anchor on and grow from an interstitial apatite plaque Randall’s plaque that covers the renal papillary surface The extent of plaque in the renal papilla has been positively correlated with urinary calcium excretion and negatively correlated with urinary volume The decreased proximal tubular reabsorption of calcium and enhanced renal tubular calcium reabsorption at the thick ascending limb have been purported as the potential pathophysiological mechanism resulting in interstitial plaque formation.
Unlike CaOx, in CaP stone formers there is apatite crystal deposition in the inner medullary collecting duct, producing plugs associated with interstitial scarring A higher percentage of kidney stones has been reported in first-degree relatives and family members with kidney stones This genetic link was further documented in a study showing a greater concordance with renal stone incidence in monozygotic than dizygotic twins However, due to the complex nature of idiopathic hypercalciuria, many putative candidate genes have been identified that participate in this polygenic illness.
Genome-wide linkage approach in three families with absorptive hypercalciuria discovered polymorphisms in the putative soluble adenylyl cyclase ADCY10 gene on chromosome 1q Another genome-wide screening in a large population from Iceland and The Netherlands with documented radio-opaque kidney stones found polymorphisms in sequence variants nelhrolithiasis the Claudin 14 CLDN14 gene, which encodes for the tight junction protein in the kidney, liver, and inner ear Another study has suggested an association between the calcium sensor receptor CASR gene polymorphism and recurrent nephrolithiasis However, none of these instances established the functional significance of these polymorphisms.
Future phenotype-genotype studies are needed to identify the associated gene defect. The etiological causes of UA stone formation are genetic, acquired, or a combination of both 60 Over the past decade, the MS has been characterized as the most prevalent cause of UA stone nephrolithiadis Fig.
The underlying pathophysiological mechanisms responsible for UA nephrolithiasis are: Causes of non-calcium kidney stone formation.
Clinical Review: Kidney Stones Pathogenesis, Diagnosis, and Management
A, UA stones; B, cystine stones; C, infectious stones. In such an acidic milieu, the urinary environment becomes supersaturated with sparingly soluble undissociated UA The two principal causes for acidic urine are: Recent experimental evidence using an established rodent model of obesity Zucher diabetic fatty rat and a renal proximal tubular cell line have demonstrated a causal role of renal steatosis in the pathogenesis of disturbed urinary acidification 86 Increased endogenous acid production has been shown in both UA stone formers and diabetic non-stone formers 84 However, the nature and source of this putative organic anion has not been fully elucidated.
Many monogenic mutations are associated with hyperuricosuria, hyperuricemia, gout, nephrolithuasis failure, and kidney stone formation 83 However, most UA stone formers have a low fractional excretion of urate and low urinary pH In one npehrolithiasis conducted in a Sardinian cohort, most subjects exhibited low urinary nephroolithiasis with hephrolithiasis urinary titratable acidity, with only one third showing elevated urinary UA excretion In this study, genetic analysis identified a locus on chromosome 10q associated nephrklithiasis increased propensity to UA nephrolithiasis.
A subsequent study identified the putative gene as zinc finger protein ZNF However, the functional importance of this finding and the role of the protein encoded by this gene have not been fully established. Cystine nephrolithiasis comprises only a small fraction of kidney stones in adults but is more prevalent among children and adolescents with stones Cystinuria is either autosomal recessive obligate heterozygotes with normal urinary cystine excretion or autosomal dominant with incomplete penetrance obligate heterozygotes with increased urinary cystine excretion but typically not enough to cause cystine stones.
Although the defective renal tubular reabsorption affects other dibasic amino acids including arginine, lysine, and ornithine, cystine stones are the main complication of this genetic defect due to the low solubility of cystine in the urinary environment Fig. In a recent genetic classification, cystinuria is defined as type A if mutations are found in both SLC3A1 nephrolithiaxis, type B if mutations are found in both SLC7A9 asoep, and type AB if one mutation is found in each gene However, cystine stones are rarely askepp in this aekep Rare forms of kidney stones such as dihydroxyadanine, ammonium urate, and stones resulting from protease inhibitor drugs may also occur.
In the diagnosis of these patients, systemic and environmental influences must be carefully identified. Systemic abnormalities include intestinal disease, disorders of calcium homeostasis such as primary hyperparathyroidism, conditions accompanied by extra renal 1,25 OH 2 D production such as granulomatous diseases, obesity, type II diabetes, recurrent urinary tract infection, bariatric surgery, medullary sponge kidney, and various drug treatments.