Cystic Diseases of the Kidney Clinical Presentation

  • Author: Thomas Patrick Frye, DO; Chief Editor: Bradley Fields Schwartz, DO, FACS   more...
 
Updated: Dec 15, 2010
 

History

  • Developmental cystic renal disease: Multicystic dysplastic kidney (MCDK) is almost uniformly identified during prenatal sonographic examination. The involved kidney partially or completely improves with age in 40-90% of patients.[9] Bilateral renal involvement is not compatible with life. MCDK can exist independently or as part of syndromes such as the vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, and radial and renal anomalies (VATER) association; Zellweger syndrome; or BOR syndrome.[10]
  • Inherited cystic renal disease
    • Autosomal dominant polycystic kidney disease
      • Patients present in the fourth decade of life with flank pain or intermittent hematuria. Patients may also experience cyst hemorrhage, renal infection, or nephrolithiasis. Hypertension and chronic renal failure are noted in the fifth decade of life, and patients progress to end-stage renal disease (ESRD) in the sixth decade of life. Hypertension is seen in 50% of patients with ADPKD aged 20-34 years.
      • The disease course varies considerably among affected individuals. While all gene carriers are believed to exhibit symptoms by the end of their eighth decade of life, only 50% of carriers actually progress to renal failure.
      • Kidney size (a direct reflection of cyst volume) increases exponentially over time and appears symmetric in a given individual, with an equal growth rate in both kidneys.[11]
      • All aspects of the disease appear to develop more rapidly in patients with the PKD1 genotype. The kidneys grow more rapidly in these patients, and hypertension and ESRD occur at a younger age; the onset of ESRD in persons with the PKD1 genotype occurs at a mean age of 53 years, while the onset of ESRD in persons with the PKD2 genotype occurs at a mean age of 69 years.[12]
      • Hepatic cysts are the most common extrarenal manifestation of autosomal dominant polycystic kidney disease (ADPKD). These increase in number with age (20% in the third decade of life, 75% after the sixth decade of life) and may cause chronic pain. However, even with extensive cystic involvement, liver function is not compromised. Other clinical associations include cardiac valve disease (particularly mitral valve prolapse [25%]), diverticulosis, cerebral aneurysms (5-10%), pancreatic cysts, and seminal vesicle cysts.[6]
    • Autosomal recessive polycystic kidney disease
      • Autosomal recessive polycystic kidney disease (ARPKD) affects renal and hepatic development (dysgenesis of the portal triad), but the degree of organ involvement varies in relation to the age of onset.
      • In the neonatal period, pulmonary disease, resulting from nephromegaly and oligohydramnios, dominates the presentation. Typically, the neonate has profound respiratory compromise, often exacerbated by pneumothorax. This presentation may result in neonatal death.
      • Symptoms in an infant include hypertension (80%), diminished urine concentrating ability, and renal insufficiency. Most affected children develop hypertension within the first few years of life. Growth retardation has been reported in one fourth of children. Fifty percent of affected individuals develop ESRD in the first decade of life, requiring dialysis or transplantation.
      • In older children (4-8 y), the kidneys often are less severely affected, while hepatic disease may predominate. Hepatic involvement usually presents with symptoms secondary to portal hypertension, particularly varices and splenomegaly. Twenty-three percent of children with ARPKD experience variceal bleeding by a mean age of 12.5 years. Hepatic disease may also result in acute bacterial cholangitis or thrombocytopenia secondary to hypersplenism.
    • Glomerulocystic kidney disease (GCKD): This occurs in early (neonatal) and late (adult) forms. Neonates present with hypertension, abdominal masses, and variable degrees of renal failure. Adults typically present with flank pain, hematuria, and hypertension. Hepatic cysts may also develop.[13]
    • Juvenile nephronophthisis (JNPHP): This has several different phenotypic expressions depending on the gene involved. Infantile (NPHP2), juvenile (NPHP1, NPHP4) and adolescent (NPHP3) forms of the disease exist, but most symptoms appear during the first decade of life. These include growth retardation, urine concentrating defects, skeletal dysplasia, and progressive renal failure. Additionally, some degree of hepatic fibrosis and biliary duct enlargement is usually present.[1]
    • Medullary cystic kidney disease: This is clinically milder than JNPHP, occurs later in life (third to fourth decades), and has limited extrarenal manifestations. Individuals with this disease due to mutations in the MCKD2 gene present with uremia sooner than those with disease due to MCKD1 mutations and are more likely to develop hyperuricemia and gout.[1]
  • Systemic disease with associated renal cysts
    • Tuberous sclerosis (TS): Clinical features of TS include facial nevi, cardiac rhabdomyomas, epilepsy, angiofibromas, and mental retardation. Approximately one half of patients have multiple renal angiomyolipomas. Twenty to 25% of patients have renal cysts, although diffuse renal cystic disease, which may result in chronic renal failure, is rare.
    • Von Hippel-Lindau syndrome (VHLS): Clinical features of VHLS include retinal and cerebellar hemangioblastomas, pheochromocytomas, and cystic disease of the kidneys, pancreas, and epididymis. Renal cysts are very common, occurring in two thirds of patients. Renal cell carcinoma (RCC) develops in as many as 40% of patients.
  • Acquired cystic renal disease
    • Acquired renal cystic disease (ARCD): Acquired cystic disease may be found in patients with all etiologies of ESRD, particularly in patients who are dialysis-dependent. The incidence, number, and size of cysts all increase in proportion to the duration of dialysis. Most patients are asymptomatic, but symptoms may include gross hematuria, flank pain, renal colic, or a palpable renal mass. Hemorrhagic cysts occur in 50% of patients.[4]
    • Medullary sponge kidney (MSK) is usually detected on radiographic evaluation of adults with nephrolithiasis. Fifteen to 20% of patients with calcium oxalate and calcium phosphate renal calculi have MSK. Patients may also have a history of hematuria or urinary tract infection (UTI). Most patients with MSK, however, are asymptomatic. Approximately 10% of patients develop recurrent nephrolithiasis, bacteriuria, and pyelonephritis. Involvement is usually bilateral.
    • Simple cysts usually are clinically silent, although they occasionally hemorrhage and cause acute pain.
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Physical

  • Developmental cystic renal disease: MCDK may be palpable as a flank mass in an otherwise healthy infant and is the most common cause of a renal mass and the second most common cause of a palpable abdominal mass in neonates.[14, 2]
  • Inherited cystic renal disease
    • ARPKD: Bilateral flank masses are palpable in 30% of neonates and infants with this disease. Older children may demonstrate signs of portal hypertension.
    • ADPKD: The enlarged kidneys and liver may be palpable.
  • Acquired cystic renal disease: Simple cysts rarely become large enough to be palpable.
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Causes

  • Developmental cystic renal disease: MCDK is thought to arise from abnormal development of the metanephros. This may be a genetic effect or may reflect a defect in the ampullary bud (inducer tissue) or the blastema (responder tissue), with resultant poor nephron induction.[2] Additionally, in utero obstruction has been identified as a possible cause, leading to urinary stasis and cyst formation. Many patients, however, have normal renal development despite obstruction.
  • Inherited cystic renal disease: Currently, the exact mechanism of genetically induced cyst formation has not been fully defined. Similarities between cystic diseases, however, reveal common pathologic pathways. The vast majority of mutations affect the primary cilia of the tubular epithelium, indicating that disruption of this structure relates to disease development.[6] Additionally, dedifferentiation and increased proliferation of tubular epithelium, along with abnormal fluid secretion, appear to be common elements in cystic disease.
    • ADPKD: Inheritance is autosomal dominant, with close to 100% penetrance. PKD1 (chromosome 16) encodes for the transmembrane protein polycystin-1 (PC1), which is responsible for cell-to-cell and cell–to–extracellular matrix binding.[6] Mutations in this gene are responsible for 85-90% of cases. Mutations in polycystin-2 (PKD2, chromosome 4), a calcium channel important for PC1 localization and function, account for the remaining 10-15%.[12] Interestingly, while this is a genetic disease that affects every cell in the kidney, cysts involve only 1-2% of the nephrons or collecting ducts, supporting the hypothesis that a "second hit," or mutation of the abnormal allele, must occur.[1] Five to 8% of cases do not involve a family history and are the result of spontaneous mutations.
    • ARPKD: Inheritance is autosomal recessive. All cases are caused by mutations in PKHD1, a large gene that encodes fibrocystin/polyductin, which appears to be related to the polycystin complex and controls epithelial proliferation, secretion, and structure and development of the renal tubules and biliary ducts.[7] The genetic defect is located on chromosome 6p21.1-p12.
    • In both ADPKD and ARPKD, epidermal growth factor (EGF) has been identified as an important stimulus for proliferation of cystic epithelium.[12]
    • GCKD is a rare disease that is transmitted in an autosomal dominant manner. The involved gene has not been identified, and both familial and sporadic forms exist.[13]
    • JNPHP is inherited in an autosomal recessive manner and is due to mutations in the NPHP genes (NPHP1-NPHP5) which are located on multiple different chromosomes and encode nephrocystins and inversin. All of the gene products are found in the primary cilium.[3, 12, 8] Ten to 20% of cases are associated with retinal disease and are termed Senior-Loken syndrome.
      • NPHP1 is located on chromosome 2q12-13 and encodes nephrocystin.
      • NPHP2 is found on chromosome 9q22-31 and encodes inversin.
      • NPHP3 is found on chromosome 3q21-22 and encodes nephrocystin-3.
      • NPHP4 is located at chromosome 1q36 and encodes nephrocystin-4.
      • NPHP5 (chromosome 3q13.33-21.2) encodes nephrocystin-5 and is found only in cases associated with Senior-Loken syndrome.
    • Medullary cystic kidney disease (MCKD) is due to mutations in the MCKD1 (chromosome 1q21) and MCKD2 (chromosome 16p12) genes and is inherited in an autosomal dominant manner.[12]
  • Systemic disease with associated renal cysts
    • TS: Inheritance is autosomal dominant, with variable penetrance. Sixty to 70% of cases are due to sporadic mutations. Genetic markers have been identified at chromosome band 9q34 (TSC1, which encodes hamartin) and chromosome band 16p13 (TSC2, which encodes tuberin). TSC2 accounts for two thirds of TS cases.[6, 1] While the functions of these genes are not understood, TSC2 is adjacent to the PKD1 gene, which is involved in the most common form of ADPKD. In some cases, a contiguous gene syndrome has been described, involving large deletions that affect both TSC2 and PKD1.
    • VHLS: Inheritance is autosomal dominant, with variable penetrance. The genetic defect has been localized to chromosome band 3p25.
  • Biochemical analyses[15, 16] have identified a protein (mTOR) that may be part of a common pathway in several of the genetic forms of cystic disease. mTOR activity is related to cell growth, proliferation, apoptosis, and differentiation. Levels of mTOR have been demonstrated to be increased in cyst epithelium. Under normal conditions, PC1 (mutated in ADPKD) and TSC2 (mutated in TS) suppress or inactivate mTOR. When these genes, as well as others that relate to the primary cilia, mutate, mTOR activity becomes dysregulated, possibly allowing cyst formation.
  • Acquired cystic renal disease: The exact cause of cyst formation has not been identified. One theory suggests that the development of cysts in acquired renal cystic disease (ARCD) is secondary to obstruction of the tubules by fibrosis or oxalate crystals. Another hypothesis invokes the accumulation of growth factors and stimulatory chemicals (uremia), including EGF, which leads to the development of cysts.[1] The disease occurs in patients on all types of dialysis and appears to regress after transplantation.
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Contributor Information and Disclosures
Author

Thomas Patrick Frye, DO  Resident

Disclosure: Nothing to disclose.

Coauthor(s)

Alex Gorbonos, MD  Assistant Professor, Division of Urology, Director, Robotic Surgery, Southern Illinois University School of Medicine

Alex Gorbonos, MD is a member of the following medical societies: Alpha Omega Alpha, American Urological Association, Endourological Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Edmund S Sabanegh Jr, MD  Director, Center for Male Fertility, Glickman Urological and Kidney Institute, Cleveland Clinic Foundation

Edmund S Sabanegh Jr, MD is a member of the following medical societies: American Medical Association, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, Society for the Study of Male Reproduction, Society of Reproductive Surgeons, and Southwest Oncology Group

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

J Stuart Wolf Jr, MD, FACS  The David A Bloom Professor of Urology, Director, Division of Endourology and Stone Disease, Department of Urology, University of Michigan Medical School

J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology

Disclosure: Baxter Healthcare Consulting fee Consulting

Chief Editor

Bradley Fields Schwartz, DO, FACS  Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine

Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Association of Military Osteopathic Physicians and Surgeons, Endourological Society, Society of Laparoendoscopic Surgeons, and Society of University Urologists

Disclosure: Nothing to disclose.

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Cut surface of a nephrectomy specimen from a patient with a multicystic dysplastic kidney (MCDK).
Nephrectomy specimen from a patient with a large benign simple cyst.
External surface of a nephrectomy specimen from a patient with autosomal dominant polycystic kidney disease (ADPKD).
Cut surface of the same nephrectomy specimen from a patient with autosomal dominant polycystic kidney disease (ADPKD).
Cut section of nephrectomy specimen demonstrating renal cell carcinoma (RCC), with an adjacent simple cyst.
Close-up photograph of the cut surface of the same nephrectomy specimen demonstrating a simple cyst adjacent to a renal cell carcinoma (RCC).
A prenatal sonogram of a fetus with a multicystic dysplastic kidney. The right kidney is appreciated as a large multicystic paraspinal mass. The left kidney and bladder are normal, and a normal amount of amniotic fluid is present.
CT examination of the abdomen of a 70-year-old woman with autosomal dominant polycystic kidney disease (ADPKD) is shown. The kidneys are bilaterally enlarged with multiple cysts.
CT scan of the same patient (70-year-old woman with autosomal dominant polycystic kidney disease [ADPKD]) demonstrating multiple hepatic cysts.
This CT scan demonstrates acquired renal cystic disease (ARCD) in a 70-year-old man who is dialysis-dependent. The CT scan demonstrates bilateral atrophic kidneys with multiple renal cysts.
A CT scan of a 38-year-old man with von Hippel-Lindau syndrome (VHLS). The patient previously underwent resection of multiple bilateral renal cell carcinomas (RCCs). CT scan demonstrates multiple cysts in the kidneys and pancreas, as well as solid renal lesions suggestive of malignancy.
 
 
 
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