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Pediatric Polycystic Kidney Disease Medication

  • Author: Priya Verghese, MD, MPH; Chief Editor: Craig B Langman, MD  more...
 
Updated: Nov 11, 2014
 

Medication Summary

Drug therapy is not currently a component of the standard of care in this condition. Medications are used only to treat the complications that arise from the disease process.

Because of the availability of animal models, preclinical trials have been developed, and promising candidate drugs have been identified for clinical trials.[13] The role of cyclic adenosine monophosphate (cAMP) in cystogenesis provided the rationale for preclinical trials of vasopressin V2 receptor antagonists. One of these drugs, OPC-31260, substantially reduced concentrations of cAMP and inhibited cyst development in models of both types of polycystic kidney disease and nephronophthisis.

An antagonist with high potency and selectivity for the human VPV2R (tolvaptan) has been shown to be an effective treatment in the rat model of autosomal recessive polycystic kidney disease and the Pkd2 mouse model of autosomal dominant polycystic kidney disease. These drugs have no effect on liver cysts. Somatostatin that acts on SST2 receptors inhibits cAMP accumulation in the kidney and in the liver. Octreotide, a synthetic, metabolically stable somatostatin analogue, halts the expansion of hepatic cysts in a rat model of polycystic kidney disease in vitro and in vivo.

Other drugs shown to be effective in preclinical trials for the treatment of human polycystic kidney disease include inhibitors of epidermal growth factor receptor, Erb-B2 tyrosine kinase, and Src kinase.[14]

Once children with autosomal recessive polycystic kidney disease develop chronic kidney disease, they require management of anemia with iron and erythropoietin; prevention of metabolic bone disease with calcium supplements, phosphate binders, and parathyroid-suppressing medication; and growth hormone to counter the growth-limiting effects of uremia.

If evidence of concentrating defects is observed in infants without significant renal insufficiency, thiazides may be useful. Bicarbonate supplements may be necessary for correction of metabolic acidosis.

Systemic hypertension should be aggressively treated with antihypertensive medication. Angiotensin-converting enzyme (ACE) inhibitors are the drugs of choice. Calcium channel blockers, beta blockers, and the judicious use of diuretics are also potential options. Antibiotics are used to treat urinary tract infections.

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Iron Salts

Class Summary

Iron salts are used to replenish iron stores. The body stores iron in compounds called ferritin and hemosiderin for future use in the production of hemoglobin. Iron absorption is a variable of the existing body iron stores, the form and quantity in foods, and the combination of foods in the diet. The ferrous form of inorganic iron is more readily absorbed.

Ferrous sulfate (Feosol, MyKidz Iron, Fer-Iron)

 

Ferrous sulfate is a source of iron for hemoglobin synthesis in the treatment of anemia of chronic renal failure. This agent is used with erythropoietin to prevent iron stores depletion. Oral solutions and chewable tablet formulations of ferrous iron salts are available for use in pediatric populations.

Sodium ferric gluconate complex (Ferrlecit, Nulecit)

 

Sodium ferric gluconate complex is used to treat microcytic hypochromic anemia due to iron deficiency when oral administration is unfeasible or ineffective as well as to replenish iron stores in individuals on erythropoietin therapy who cannot take or tolerate oral iron supplementation.

Iron sucrose (Venofer)

 

Iron sucrose is a polynuclear iron (III) hydroxide in sucrose for intravenous use. This agent contains no preservatives or dextran polysaccharides. Iron sucrose is used to treat microcytic hypochromic anemia due to iron deficiency when oral administration is unfeasible or ineffective, as well as to replenish iron stores in individuals on erythropoietin therapy who cannot take or tolerate oral iron supplementation.

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Colony Stimulating Factors

Class Summary

Colony stimulating factors are used to stimulate blood cell production. Endogenous erythropoietin stimulates red blood cell (RBC) hematopoiesis. Recombinant human erythropoietin (epoetin alfa) and darbepoetin stimulate erythropoiesis in anemic conditions.

Epoetin alfa (Epogen, Procrit)

 

Epoetin alfa stimulates the division and differentiation of committed erythroid progenitor cells and induces the release of reticulocytes from the bone marrow into the blood stream.

Darbepoetin alfa (Aranesp)

 

Darbepoetin alfa stimulates the division and differentiation of committed erythroid progenitor cells and induces the release of reticulocytes from the bone marrow into the blood stream.

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Phosphate Binders

Class Summary

Phosphate binding agents are indicated if phosphate elevation is uncontrolled by dietary phosphate restriction. Calcium phosphate binders are typically the initial therapy for hyperphosphatemia. Calcium supplements and calcitriol may also possibly be used for hypocalcemia.

Calcium acetate (Eliphos, PhosLo)

 

Calcium acetate is indicated for the treatment of hyperphosphatemia secondary to chronic renal failure. This agent combines with dietary phosphorus to form insoluble calcium phosphate, which is excreted in feces. One caplet or tablet of calcium acetate 667 mg is equivalent to 169-mg elemental calcium (ie, 1 g calcium acetate equivalent to 250-mg of elemental calcium).

Calcium carbonate (Caltrate, Tums, Alcalak)

 

Calcium carbonate is used to treat hyperphosphatemia in chronic renal failure. This agent combines with dietary phosphorus to form insoluble calcium phosphate, which is excreted in feces. Calcium carbonate is also indicated for hypocalcemia. Calcium carbonate 1 g is equivalent to 400 mg of elemental calcium.

Sevelamer (Renagel, Renvela)

 

Sevelamer is indicated to reduce serum phosphorous in patients with end-stage renal disease (ESRD). This agent binds dietary phosphate in the intestine, thus inhibiting its absorption as well as reduces the incidence of hypercalcemic episodes in patients on hemodialysis compared with patients receiving calcium acetate treatment.

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Vitamin D Analogues

Class Summary

Hyperparathyroidism is treated with calcitriol or other active vitamin D analogues. These drugs may also be used to treat hypocalcemia.

Calcitriol (Rocaltrol, Calcijex, Vectical)

 

Calcitriol is a primary active metabolite of vitamin D-3. This agent increases calcium levels in serum by promoting absorption of calcium in the intestines and retention in the kidneys. Calcitriol decreases excessive serum phosphatase levels and parathyroid levels as well as decreases bone resorption.

Calcitriol should be used in patients with renal failure who are unable to convert the inactive prohormone forms to the active metabolite. This agent is available in oral and parenteral formulations. This active form of vitamin D is used in cases of proximal renal tubular acidosis (pRTA) as multitherapy with large quantities of alkali and potassium supplementation and is also used to suppress parathyroid production and secretion in secondary hyperparathyroidism and for treatment of hypocalcemia in chronic renal failure by increasing intestinal calcium absorption.

Paricalcitol (Zemplar)

 

Paricalcitol, an active form of vitamin D, is formed through the removal of the 19th carbon group and modifications to the side chain of calcitriol, thus reducing the calcemic effect. This agent has been reported to suppress parathyroid hormone (PTH) without significant impact on calcium, phosphorus, or calcium-phosphorus product. Paricalcitol increases calcium levels in serum by promoting absorption of calcium in intestines and retention in kidneys, decreases excessive serum phosphatase levels and PTH levels, and decreases bone resorption.

This agent should be used in patients with renal failure who are unable to convert the inactive prohormone forms to the active metabolite. It is also used to suppress parathyroid production and secretion in secondary hyperparathyroidism and for treatment of hypocalcemia in chronic renal failure by increasing intestinal calcium absorption. Paricalcitol is available in oral and parenteral formulations.

Doxercalciferol (Hectorol)

 

Doxercalciferol is a vitamin D analogue (1-alpha-hydroxyergocalciferol) that does not require activation by the kidneys but does require hydroxylation in the liver to be converted to an active vitamin D metabolite. This agent controls intestinal absorption of dietary calcium, tubular reabsorption of calcium by the kidneys, and in conjunction with parathyroid hormone, the mobilization of calcium from skeleton. Doxercalciferol is indicated for the treatment of secondary hyperparathyroidism in end-stage renal disease (ESRD).

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Growth Hormones

Class Summary

Growth hormones are used pharmacologically as growth-promoting agents to help optimize growth in developing children with chronic kidney disease (CKD).

Growth hormone (Nutropin, Saizen, Genotropin)

 

Growth hormone is a human growth hormone (hGH) produced by recombinant DNA technology and whose use results in stimulation of linear growth. This agent stimulates erythropoietin, which increases red blood cell mass.

Growth hormone is currently widely available in subcutaneous (SC) injection form. Adjust the dose gradually based on clinical and biochemical responses assessed at monthly intervals, including body weight, waist circumference, serum insulinlike growth factor-1 (IGF-1), insulinlike growth factor binding protein-3 (IGFBP-3), serum glucose, lipids, thyroid function, and whole body dual-energy x-ray absorptiometry (DEXA). In children, assess treatment response based on height and growth velocity. Continue treatment until the child's final height or epiphysial closure or both have been recorded.

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Calcimimetic Agents

Class Summary

Calcimimetic agents reduce parathyroid hormone (PTH) levels.

Cinacalcet (Sensipar)

 

Cinacalcet directly lowers intact parathyroid hormone (iPTH) levels by increasing the sensitivity of the calcium-sensing receptor on chief cell of the parathyroid gland to extracellular calcium. This process also results in concomitant serum calcium decrease. Cinacalcet is indicated for secondary hyperparathyroidism in patients with chronic kidney disease on dialysis.

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Diuretic Agents

Class Summary

These agents are used to remove excess fluid in children with edema secondary to renal disease and are administered as an adjunct to manage hypertension and excess fluid.

Furosemide (Lasix)

 

Furosemide is a loop diuretic. It is often effective in removing fluid even when the glomerular filtration rate is reduced secondary to nephritis. This agent increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.

Hydrochlorothiazide (Microzide)

 

Hydrochlorothiazide (HCTZ) acts on the distal nephron to impair sodium reabsorption, enhancing sodium excretion. It has been in use for more than 40 years and is generally an important agent for the treatment of essential hypertension.

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ACE Inhibitors

Class Summary

These agents reduce the systemic arterial blood pressure, reducing injury caused by elevated blood pressure. They may not only reduce cardiovascular risk but also slow progression of renal failure. ACE inhibitors may also slow progression of renal failure by lowering intraglomerular pressure or other intrarenal mechanisms.

A dry cough is a common adverse effect of ACE inhibitors. If the cough occurs with one ACE inhibitor, it is likely to occur with another. A reasonable substitute for an ACE inhibitor if a cough develops is an ARB, such as losartan, valsartan, or candesartan.

Captopril

 

Captopril, a competitive ACE inhibitor, prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, increasing levels of plasma renin and reducing aldosterone secretion. It has been clinically used for more than 20 years and is effective in experimental radiation nephropathy. Captopril may slow the progression of renal failure by lowering intraglomerular pressure or other intrarenal mechanisms.

Enalapril (Vasotec)

 

A competitive ACE inhibitor, enalapril reduces angiotensin II levels, decreasing aldosterone secretion. The drug lowers systemic arterial blood pressure, reducing injury caused by elevated blood pressure. It may slow the progression of renal failure by lowering intraglomerular pressure or other intrarenal mechanisms. Enalapril may be used every day or twice per day, which may improve compliance in comparison with a 3-time-per-day medication, such as captopril.

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Angiotensin II Receptor Antagonists

Class Summary

ARBs antagonize the action of angiotensin II at the type 1 receptor, reducing systemic arterial blood pressure and blunting the intrarenal effect of angiotensin II. If ACE inhibitors cause cough, ARBs may be substituted.

Losartan (Cozaar)

 

Losartan is a prototype ARB. It is specific for the type 1, as opposed to type 2, angiotensin receptor. It may induce more complete inhibition of the renin-angiotensin system than do ACE inhibitors. Losartan does not appear to affect bradykinin and is less likely to be associated with cough and angioedema. Use it in patients who are unable to tolerate ACE inhibitors.

Valsartan (Diovan)

 

Valsartan is a prodrug that directly antagonizes angiotensin II receptors. It displaces angiotensin II from the AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. Valsartan may induce more complete inhibition of the renin-angiotensin system than do ACE inhibitors. It does not affect bradykinin and is less likely to be associated with cough and angioedema. Valsartan is for use in patients who are unable to tolerate ACE inhibitors.

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Calcium Channel Blockers

Class Summary

Antihypertensive agents other than or in addition to ACE inhibitors and ARBs may be needed for blood pressure control in many subjects with hypertension and chronic renal failure. The same is true for subjects with radiation nephritis. No evidence indicates that one type of calcium channel blocker is preferred over another for radiation nephritis. However, one should avoid verapamil, because the use of this drug in a subject with hyperkalemia may cause atrial arrest.

Nifedipine (Procardia, Adalat, Nifedical XL)

 

Like other calcium channel blockers, nifedipine causes peripheral arterial vasodilation by inhibiting calcium influx across vascular smooth-muscle cell membranes. Long-acting formulations are used for control of blood pressure.

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Beta Adrenergic Blockers

Class Summary

These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation

Esmolol (Brevibloc)

 

An ultra–short-acting beta-1-blocker, esmolol is particularly useful in patients with elevated arterial pressure, especially if surgery is planned. It may be useful as a means to test beta-blocker safety and tolerance in patients with history of obstructive pulmonary disease who are at uncertain risk for bronchospasm from beta-blockade. The elimination half-life of esmolol is 9 min.

Labetalol (Trandate)

 

Labetalol blocks alpha-1 beta 1-, and beta 2-adrenergic receptor sites, decreasing BP.

Propranolol (Inderal, InnoPran XL)

 

A class II antiarrhythmic nonselective beta-adrenergic receptor blocker, propranolol has membrane-stabilizing activity and decreases automaticity of contractions. Propranolol is not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies.

Metoprolol (Lopressor, Toprol-XL)

 

Metoprolol is a selective beta 1–adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG. When considering conversion from IV to oral (PO) dosage forms, use the ratio of 2.5 mg PO to 1 mg IV metoprolol.

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Alkalinizing Agents

Class Summary

Sodium bicarbonate is used as a gastric, systemic, and urinary alkalinizer and has been used in the treatment of acidosis resulting from metabolic and respiratory causes, including, diarrhea, kidney disturbances, and shock. Alternatively, THAM is a buffering agent that increases pH without increasing levels of PaCO2. It may be used to correct metabolic acidosis if sodium bicarbonate is contraindicated.

Sodium bicarbonate

 

Sodium bicarbonate serves as a buffering agent for metabolic acidosis when significant bicarbonate losses have occurred.

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Contributor Information and Disclosures
Author

Priya Verghese, MD, MPH Fellow in Pediatric Nephrology, Seattle Children's Hospital, University of Washington School of Medicine

Priya Verghese, MD, MPH is a member of the following medical societies: American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

Henrique M Lederman, MD, PhD Consulting Staff, Department of Radiology, LeBonheur Children's Medical Center and St Jude Children's Research Hospital; Professor of Radiology and Pediatric Radiology, Chief, Division of Diagnostic Imaging in Pediatrics, Federal University of Sao Paulo, Brazil

Henrique M Lederman, MD, PhD is a member of the following medical societies: Society for Pediatric Radiology

Disclosure: Nothing to disclose.

Jordan M Symons, MD Associate Professor of Pediatrics, University of Washington School of Medicine; Director of the Acute Dialysis Program, Seattle Children's Hospital

Jordan M Symons, MD is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology, Renal Physicians Association

Disclosure: Nothing to disclose.

José Luiz de Oliveira Schiavon, MD Associate Professor, Department of Pediatric Radiology, Instituto de Oncologia Pediatrica, Universidade Federal De Sao Paulo, Brazil

José Luiz de Oliveira Schiavon, MD is a member of the following medical societies: Radiological Society of North America

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Luther Travis, MD Professor Emeritus, Departments of Pediatrics, Nephrology and Diabetes, University of Texas Medical Branch School of Medicine

Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, Texas Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

Richard Neiberger, MD, PhD Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical and Dental Associations, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors H Jorge Baluarte, MD, and Peter J Hurh, MD,to the development and writing of the source article.

References
  1. OSATHANONDH V, POTTER EL. PATHOGENESIS OF POLYCYSTIC KIDNEYS. TYPE 1 DUE TO HYPERPLASIA OF INTERSTITIAL PORTIONS OF COLLECTING TUBULES. Arch Pathol. 1964 May. 77:466-73. [Medline].

  2. OSATHANONDH V, POTTER EL. PATHOGENESIS OF POLYCYSTIC KIDNEYS. HISTORICAL SURVEY. Arch Pathol. 1964 May. 77:459-65. [Medline].

  3. Grantham JJ, Torres VE, Chapman AB, et al. Volume progression in polycystic kidney disease. N Engl J Med. 2006 May 18. 354(20):2122-30. [Medline].

  4. Yoder BK, Mulroy S, Eustace H, Boucher C, Sandford R. Molecular pathogenesis of autosomal dominant polycystic kidney disease. Expert Rev Mol Med. 2006 Jan 17. 8(2):1-22. [Medline].

  5. Sweeney WE Jr, Avner ED. Molecular and cellular pathophysiology of autosomal recessive polycystic kidney disease (ARPKD). Cell Tissue Res. 2006 Dec. 326(3):671-85. [Medline].

  6. Zerres K, Mücher G, Bachner L, et al. Mapping of the gene for autosomal recessive polycystic kidney disease (ARPKD) to chromosome 6p21-cen. Nat Genet. 1994 Jul. 7(3):429-32. [Medline].

  7. Sharp AM, Messiaen LM, Page G, et al. Comprehensive genomic analysis of PKHD1 mutations in ARPKD cohorts. J Med Genet. 2005 Apr. 42(4):336-49. [Medline]. [Full Text].

  8. Gunay-Aygun M, Avner ED, Bacallao RL, et al. Autosomal recessive polycystic kidney disease and congenital hepatic fibrosis: summary statement of a first National Institutes of Health/Office of Rare Diseases conference. J Pediatr. 2006 Aug. 149(2):159-64. [Medline]. [Full Text].

  9. O'Brien K, Font-Montgomery E, Lukose L, et al. Congenital hepatic fibrosis and portal hypertension in autosomal dominant polycystic kidney disease. J Pediatr Gastroenterol Nutr. 2012 Jan. 54(1):83-9. [Medline].

  10. Gunay-Aygun M, Font-Montgomery E, Lukose L, Tuchman Gerstein M, Piwnica-Worms K, Choyke P, et al. Characteristics of congenital hepatic fibrosis in a large cohort of patients with autosomal recessive polycystic kidney disease. Gastroenterology. 2013 Jan. 144(1):112-121.e2. [Medline]. [Full Text].

  11. Boyer O, Gagnadoux MF, Guest G, et al. Prognosis of autosomal dominant polycystic kidney disease diagnosed in utero or at birth. Pediatr Nephrol. 2007 Mar. 22(3):380-8. [Medline].

  12. Bajwa ZH, Sial KA, Malik AB, Steinman TI. Pain patterns in patients with polycystic kidney disease. Kidney Int. 2004 Oct. 66(4):1561-9. [Medline]. [Full Text].

  13. Chapman AB. Approaches to testing new treatments in autosomal dominant polycystic kidney disease: insights from the CRISP and HALT-PKD studies. Clin J Am Soc Nephrol. 2008 Jul. 3(4):1197-204. [Medline].

  14. Sweeney WE, Chen Y, Nakanishi K, et al. Treatment of polycystic kidney disease with a novel tyrosine kinase inhibitor. Kidney Int. 2000 Jan. 57(1):33-40. [Medline].

 
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Sonogram shows cysts with bilaterally enlarged kidneys. These findings are compatible with a diagnosis of autosomal dominant polycystic kidney disease (ADPKD).
Sonogram shows cysts with bilaterally enlarged kidneys. These findings are compatible with a diagnosis of autosomal dominant polycystic kidney disease (ADPKD).
Sonogram shows cysts with bilaterally enlarged kidneys. These findings are compatible with a diagnosis of autosomal dominant polycystic kidney disease (ADPKD).
Frontal excretory urogram of autosomal dominant polycystic kidney disease (ADPKD) shows a spider-legs configuration of the collecting system secondary to compression due to cysts.
Lateral excretory urogram of autosomal dominant polycystic kidney disease (ADPKD) shows a spider-legs configuration of the collecting system secondary to compression due to cysts.
Pathologic specimen of end-stage autosomal dominant polycystic kidney disease (ADPKD) with deformed lobulated kidneys.
Sonogram shows enlargement of both kidneys, diffuse increased echogenicity, and loss of corticomedullary differentiation. These findings are compatible with a diagnosis of autosomal recessive polycystic kidney disease (ARPKD).
Excretory urogram shows minimal bilateral tubular changes caused by a mild form of autosomal recessive polycystic kidney disease (ARPKD).
Excretory urogram shows enlarged kidneys with bilateral distortion of the collecting system (spider-legs configuration). These findings are compatible with a diagnosis of autosomal recessive polycystic kidney disease (ARPKD).
Excretory urogram shows the typical mottled (spongelike) contrast pattern in autosomal recessive polycystic kidney disease (ARPKD).
Excretory urogram shows the typical mottled (spongelike) contrast pattern in autosomal recessive polycystic kidney disease (ARPKD).
Excretory urogram shows the typical mottled (spongelike) contrast enhancement pattern in autosomal recessive polycystic kidney disease (ARPKD).
CT shows bilaterally smooth enlarged kidneys. These findings are compatible with a diagnosis of autosomal recessive polycystic kidney disease (ARPKD).
CT shows bilateral renal and liver cysts with enlarged kidneys and remaining renal cortex enhancement compatible with a diagnosis of autosomal dominant polycystic kidney disease (ADPKD).
T2-weighted MRI shows bilateral smooth enlarged kidneys with a hyperintense, linear, radial pattern in the cortex and medulla, compatible with autosomal recessive kidney disease.
T1- and T2-weighted MRIs demonstrating a superior left kidney cyst with high T1 and intermediary T2 signal compatible with a bleeding cyst in autosomal dominant polycystic kidney disease (ADPKD).
T1- and T2-weighted MRIs demonstrating bilateral renal and liver cysts compatible with autosomal dominant polycystic kidney disease (ADPKD).
 
 
 
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