The Effect of Caffeine on Renal Epithelial Cells from Patients with Autosomal Dominant Polycystic Kidney Disease

Belibi, Franck A.; Wallace, Darren P.; Yamaguchi, Tomohiro; Christensen, Marcy; Reif, Gail A.; Grantham, Jared J.

doi:10.1097/01.asn.0000025282.48298.7b

Cited by 99 publications

(76 citation statements)

References 33 publications

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“…96 High caffeine intake may, therefore, be a risk factor for cyst enlargement and ADPKD progression, although a small clinical study has suggested no correlation between mild caffeine intake and TKV by ultrasound. 97 Nevertheless, it is recommended to counsel patients with ADPKD to limit their caffeine intake.…”

Section: Birth Weightmentioning

confidence: 99%

Predictors of Autosomal Dominant Polycystic Kidney Disease Progression

Schrier

Brosnahan

Cadnapaphornchai

et al. 2014

Journal of the American Society of Nephrology

145

120

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Autosomal dominant polycystic kidney disease is a genetic disorder associated with substantial variability in its natural course within and between affected families. Understanding predictors for rapid progression of this disease has become increasingly important with the emergence of potential new treatments. This systematic review of the literature since 1988 evaluates factors that may predict and/or effect autosomal dominant polycystic kidney disease progression. Predicting factors associated with early adverse structural and/or functional outcomes are considered. These factors include PKD1 mutation (particularly truncating mutation), men, early onset of hypertension, early and frequent gross hematuria, and among women, three or more pregnancies. Increases in total kidney volume and decreases in GFR and renal blood flow greater than expected for a given age also signify rapid disease progression. Concerning laboratory markers include overt proteinuria, macroalbuminuria, and perhaps, elevated serum copeptin levels in affected adults. These factors and others may help to identify patients with autosomal dominant polycystic kidney disease who are most likely to benefit from early intervention with novel treatments.

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Section: Birth Weightmentioning

confidence: 99%

Predictors of Autosomal Dominant Polycystic Kidney Disease Progression

Schrier

Brosnahan

Cadnapaphornchai

et al. 2014

Journal of the American Society of Nephrology

145

120

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“…The additional water should be free of caffeine (77) and sugar (78) and contain vanishingly low amounts of dichloroacetate (79) and fluoride (80). A reasonable goal is to drink fluids as evenly as possible throughout waking hours and immediately before going to bed.…”

Section: Which Adpkd Patients Can Safely Increase Water Intake and Homentioning

confidence: 99%

A Case for Water in the Treatment of Polycystic Kidney Disease

Torres¹,

Bankir²,

Grantham³

2009

Clinical Journal of the American Society of Nephrology

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130

101

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Autosomal dominant polycystic disease (ADPKD) is an inherited disorder characterized by the development within renal tubules of innumerable cysts that progressively expand to cause renal insufficiency. Tubule cell proliferation and transepithelial fluid secretion combine to enlarge renal cysts, and 3-5-cyclic adenosine monophosphate (cAMP) stimulates that growth. The antidiuretic hormone, arginine vasopressin (AVP), operates continuously in ADPKD patients to stimulate the formation of cAMP, thereby contributing to cyst and kidney enlargement and renal dysfunction. Studies in animal models of ADPKD provide convincing evidence that blocking the action of AVP dramatically ameliorates the disease process. In the current analysis, the authors reason that increasing the amount of solute-free water drunk evenly throughout the day in patients with ADPKD and normal renal function will decrease plasma AVP concentrations and mitigate the action of cAMP on the renal cysts. Potential pitfalls of increasing fluid intake in ADPKD patients are considered, and suggestions for how physicians may prudently implement this therapy are offered.Clin J Am Soc Nephrol 4: 1140 -1150, 2009. doi: 10.2215/CJN.00790209 C onvergent findings in the last decade have established that 3Ј-5Ј-cyclic adenosine monophosphate (cAMP) stimulates mural epithelial cell proliferation and secretion of fluid into cysts of patients with autosomal dominant polycystic kidney disease (ADPKD), contributing to massive renal enlargement and dysfunction (1). AVP promotes cAMP production in the distal nephron and collecting ducts (CDs) by acting on AVP-V2 receptors (V2R). Preclinical evidence has shown in four different genetic models of polycystic kidney disease (PKD) that blocking the effect of AVP, thereby decreasing cAMP levels, slows cyst and renal enlargement and improves renal function (2-4).A novel treatment for ADPKD that targets AVP/cAMP is currently being evaluated in an international clinical trial (TEMPO NCT00428948). An inhibitor of V2R (tolvaptan) is administered to patients with the intent to diminish intracellular cAMP levels in cyst epithelial cells. V2R inhibition also diminishes the reabsorption of solute-free water in CDs, thereby causing partial nephrogenic diabetes insipidus and thirst. Daily urine volumes 5 d after starting different split doses of tolvaptan (15/15, 30/0, 30/15, 30/30 mg) in a preliminary phase 2 study were 4 to 6 L (5). This polyuria requires ingestion of enough water to maintain normal fluid balance, and TEMPO trial participants are instructed to drink enough to prevent or minimize thirst.Another way to decrease the effect of AVP on the kidney is to suppress its secretion by increasing fluid ingestion above what normal thirst would command. This strategy is hardly new, as a high fluid intake to dilute the urine likely is the oldest existing treatment in nephrology. Up to 3000 cc of water per day, drunk relatively evenly throughout waking hours and before going to bed, is frequently recommended to prevent urine supersaturatio...

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“…The faster growth of kidney cysts in male individuals with ADPKD and also earlier ESRD in male individuals with PKD2 suggest that male hormonal factors may be important in renal cystic disease (20,43). Caffeine exposure has been considered a risk factor in PKD, and evidence that caffeine can increase the production of cAMP in cyst-derived cells, which stimulate proliferation and fluid secretion (72), provides some justification for avoiding caffeinecontaining beverages. Smoking has been shown to be a risk factor for more rapid progression in patients with renal disease, including ADPKD, with increased risk for chronic renal failure and ESRD, especially in men (73).…”

Section: Environmental Influencesmentioning

confidence: 99%

Genotype–Phenotype Correlations in Autosomal Dominant and Autosomal Recessive Polycystic Kidney Disease

Rossetti¹,

Harris²

2007

Journal of the American Society of Nephrology

174

119

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The phenotypes that are associated with the common forms of polycystic kidney disease (PKD)-autosomal dominant (ADPKD) and autosomal recessive (ARPKD)-are highly variable in penetrance. This is in terms of severity of renal disease, which can range from neonatal death to adequate function into old age, characteristics of the liver disease, and other extrarenal manifestations in ADPKD. Influences of the germline mutation are at the genic and allelic levels, but intrafamilial variability indicates that genetic background and environmental factors are also key. In ADPKD, the gene involved, PKD1 or PKD2, is a major factor, with ESRD occurring 20 yr later in PKD2. Mutation position may also be significant, especially in terms of the likelihood of vascular events, with 5 mutations most detrimental. Variance component analysis in ADPKD populations indicates that genetic modifiers are important, but few such factors (beyond co-inheritance of a TSC2 mutation) have been identified. Hormonal influences, especially associated with more severe liver disease in female individuals, indicate a role for nongenetic factors. In ARPKD, the combination of mutations is critical to the phenotypic outcome. Patients with two truncating mutations have a lethal phenotype, whereas the presence of at least one missense change can be compatible with life, indicating that many missense changes are hypomorphic alleles that generate partially functional protein. Clues from animal models and other forms of PKD highlight potential modifiers. The information that is now available on both genes is of considerable prognostic value with the prospects from the ongoing genetic revolution that additional risk factors will be revealed.

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The Effect of Caffeine on Renal Epithelial Cells from Patients with Autosomal Dominant Polycystic Kidney Disease

Cited by 99 publications

References 33 publications

Predictors of Autosomal Dominant Polycystic Kidney Disease Progression

Predictors of Autosomal Dominant Polycystic Kidney Disease Progression

A Case for Water in the Treatment of Polycystic Kidney Disease

Genotype–Phenotype Correlations in Autosomal Dominant and Autosomal Recessive Polycystic Kidney Disease

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