The 5 Minute Urology Consult 3rd Ed.

MEDULLARY CYSTIC KIDNEY DISEASE (MCKD)

Scott G. Hubosky, MD

BASICS

DESCRIPTION

• Medullary cystic kidney disease (MCKD) is a rare congenital, cystic disease of the kidneys which results in progressive renal deterioration and to eventual end-stage renal disease (ESRD)

• Symptoms develop insidiously and diagnosis is not common until renal insufficiency is detected and initiates evaluation (1)[C]

EPIDEMIOLOGY

Incidence

Less than 1: 100,000

Prevalence

N/A

RISK FACTORS

Positive family history

Genetics

• Mode of inheritance is autosomal dominant (2)[C]

– Medullary cystic kidney disease-1 (MCKD1)

Mutation in MCKD1 gene localized to chromosome 1q21

– MCKD2

Mutation in MCKD2 gene localized to chromosome 16p12

PATHOPHYSIOLOGY

• Unlike other renal cystic diseases such as autosomal dominant polycystic kidney disease (ADPKD), there is no clear correlation between genetic mutation and identifiable protein product responsible for the MCKD phenotype (3)[C]

ASSOCIATED CONDITIONS

• Hyperuricemia and gouty arthritis are associated with MCKD2

• In contrast to juvenile nephronophthisis, MCKD does not have many extrarenal manifestations

GENERAL PREVENTION

N/A

DIAGNOSIS

HISTORY

• Polyuria

– Usually the 1st clinical manifestation

– Occurs due to reduced urinary concentrating ability of the kidney

• Polydipsia

• Family history of ESRD, or renal cysts

PHYSICAL EXAM

Hypertension may be noted with disease progression

DIAGNOSTIC TESTS & INTERPRETATION

Lab

• Urinalysis

– Proteinuria and hematuria are usually absent

• CBC

– Anemia present in advanced cases due to lack of erythropoietin

• Serum electrolytes

– Elevated creatinine

– Hyperkalemia or metabolic acidosis in later stages due to renal insufficiency

Imaging

• Renal ultrasound

– Kidneys may be atrophic depending on stage of disease

– Cysts may be visible at the corticomedullary junction in later disease but are usually not detectable in early stages

– Increased parenchymal echogenicity from tubulointerstitial fibrosis

• CT scan

– Can detect cysts at the corticomedullary junction better than ultrasound

– Need for IV contrast is suboptimal in patients with ESRD

Diagnostic Procedures/Surgery

Percutaneous renal biopsy confirms the diagnosis

Pathologic Findings

• Gross findings

– Initially before disease progression, the kidneys are of normal size

– Cortical atrophy with progression

– Cysts develop at the corticomedullary junction and range in size from 1 to 10 mm.

– With disease advancement the kidneys become very small and demonstrate a granular exterior surface

• Microscopic findings

– Interstitial nephritis

– Dilated, atrophic tubules

– Inflammatory cell infiltrates

DIFFERENTIAL DIAGNOSIS

• Juvenile nephronophthisis

– Clinically and anatomically similar to MCKD

– Autosomal recessive inheritance

– ESRD usually manifests as early as age 13 yr

– Extrarenal manifestations are common

Retinal disorders (retinitis pigmentosa)

Hepatic fibrosis

Bardet–Biedl syndrome (obesity, retinitis pigmentosa, mental retardation, polydactyly)

• Polycystic kidney disease

– Autosomal recessive polycystic kidney disease (infantile form)

– Autosomal dominant polycystic kidney disease (adult form)

• Multicystic dysplastic kidney

• Benign multilocular cyst (cystic nephroma)

• Medullary sponge kidney

TREATMENT

GENERAL MEASURES

• Same as for any patient with renal insufficiency

– Control hypertension if present

– Monitor fluid balance/daily weights

– Monitor serum electrolytes

MEDICATION

First Line

• None for primary treatment

• Antihypertensive regimens sometimes necessary

Second Line

N/A

SURGERY/OTHER PROCEDURES

• Dialysis when ESRD develops

• Renal transplant

– Allograft is not affected by MCKD after transplantation

ADDITIONAL TREATMENT

Radiation Therapy

N/A

Additional Therapies

N/A

Complementary & Alternative Therapies

N/A

ONGOING CARE

PROGNOSIS

• MCKD1 patients manifest with ESRD at median age of 62 yr

• MCKD2 patients manifest with ESRD at median age of 32 yr

COMPLICATIONS

Similar to any patient with renal insufficiency or ESRD

FOLLOW-UP

Patient Monitoring

Close nephrology follow-up is essential

Patient Resources

• National Kidney Foundation

www.kidney.org/patients

REFERENCES

1. Scolari F, Ghiggeri GM. Nephronophthisis-medullary cystic kidney disease: From bedside to bench and back again. Saudi J Kidney Dis Transplant. 2003;14:316–327.

2. Hildebrandt F, Omram H. New Insights: Nephronophthisis-medullary cystic kidney disease. Pediatr Nephrol. 2001;16:168–176.

3. Kim CM, Glassberg KI. Molecular mechanisms of renal development. Cur Urol Rep. 2003;4:164–170.

ADDITIONAL READING

Hildebrandt F, Otto E. Molecular genetics of nephronophthisis and medullary cystic kidney disease. J Am Soc Nephrol. 2000;11:1753–1761.

See Also (Topic, Algorithm, Media)

• Nephronophthisis (Juvenile, Infantile, and Adolescent)

• Renal Cysts (Intrarenal, Peripelvic, and Parapelvic)

• Renal Mass

CODES

ICD9

• 585.6 End stage renal disease

• 753.16 Medullary cystic kidney

• 788.42 Polyuria

ICD10

• N18.6 End stage renal disease

• Q61.5 Medullary cystic kidney

• R35.8 Other polyuria

CLINICAL/SURGICAL PEARLS

• MCKD has an insidious disease onset.

• Symptoms usually not present until patient has renal insufficiency documented on serum testing.

• Polyuria is commonly the 1st clinical manifestation.



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