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A autosomal dominant polycystic kidney disease that has material basis in mutation in the PKD4 gene.
Features include very common findings: Liver scarring (fibrosis) (hepatic fibrosis) and Renal cyst; and common findings: Hyperechogenic kidneys and Hypertension. 22 total HPO annotations.
Organ System | Phenotype Count | Example Features |
|---|---|---|
Kidneys and urinary system | 8 | Tubulointerstitial fibrosis, Reduced kidney function (renal insufficiency), Hyperechogenic kidneys |
Digestive system | 6 | Liver scarring (fibrosis) (hepatic fibrosis), Enlarged liver (hepatomegaly), Esophageal varix |
Heart and blood vessels | 2 | Portal hypertension, Hypertension |
Lungs and breathing | 1 | Pulmonary hypoplasia |
Blood and immune system | 1 | Enlarged spleen (splenomegaly) |
Autosomal recessive polycystic kidney disease – PKHD1 (ARPKD-PKHD1) is characterized by primary involvement of the kidneys and liver with secondary effects seen in other organ systems [, , , , , ]. Of the three ages of initial presentation of kidney disease, the two most common are perinatal (i.e., prenatal/neonatal) and infantile (four weeks to age one year) with the classic finding of enlarged kidneys. While the perinatal and infantile presentations typically have similar kidney and liver findings, the major difference between the two is the frequent occurrence of pulmonary involvement in the perinatal presentation. The less common initial presentation in childhood (after age one year) to young adulthood can be associated with predominant hepatobiliary manifestations characterized by developmental anomalies of biliary ductal plate remodeling, also known as congenital hepatic fibrosis (CHF). See for a comparison of clinical findings at presentation by age at presentation. Note: (1) Because some data on ARPKD predates the understanding of its heterogeneous genetic causes, information in this section is based on study cohorts with ARPKD in general as well as cohorts with ARPKD-PKHD1 . (2) Although the ARPKD phenotype appears to be clinically similar regardless of the causative gene, the genetic etiology may be relevant for prognosis of kidney survival (i.e., time to onset of kidney replacement therapy) . Table 2. Autosomal Recessive Polycystic Kidney Disease: Comparison of Clinical Findings at Presentation by Age at Presentation Feature | Age at Presentation
Perinatal |
|---|
PKHD1 function has not been fully characterized.
Polycystic kidney disease 4 is associated with mutations in the PKHD1 gene on chromosome 6.
In ARPKD-PKHD1 several genotype-phenotype correlations have been observed based on class of the pathogenic variant and location within the fibrocystin protein (see and , respectively) . Importantly, no statistically significant differences for kidney survival (i.e., time to onset of KRT) were found during childhood and adolescence when comparing subgroups of individuals stratified according to their molecular diagnosis .
Table 3a.
Autosomal Recessive Polycystic Kidney Disease – PKHD1: Genotype-Phenotype Correlations by Variant Class
PKHD1 Variant Class | Genotype-Phenotype Correlation | Comment
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
Consensus expert recommendations for the clinical diagnosis of autosomal recessive polycystic kidney disease (ARPKD) were published in 2014 .
Autosomal recessive polycystic kidney disease – PKHD1 (ARPKD-PKHD1) should be suspected in probands with the following age-related clinical and ultrasonographic findings at presentation and family history. Note: (1) Ultrasonography is the imaging method of choice for assessing the kidneys prenatally and in all pediatric age groups because it is cost-effective, painless, widely available, and does not require radiation or sedation. (2) Kidney biopsies should not be performed to diagnose ARPKD.
Perinatal Presentation (prenatal to age 4 weeks)
Kidney
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
Autosomal recessive polycystic kidney disease (ARPKD) belongs to a group of congenital hepatorenal fibrocystic syndromes and is a cause of significant kidney- and liver-related morbidity and mortality in children. Among individuals with ARPKD, PKHD1 is the most commonly involved gene. ARPKD caused by pathogenic variants in PKHD1 (i.e., ARPKD-PKHD1) must be distinguished from the following :
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
Genetic testing for PKHD1 is available. Testing is considered confirmatory for diagnosis.
Biomarker and diagnostic research for polycystic kidney disease 4 has been reported in the published literature.
No approved treatments are currently available for polycystic kidney disease 4. The disease remains an area of unmet medical need.
Consensus expert recommendations for the management of autosomal recessive polycystic kidney disease (ARPKD) and clinical practice recommendations for perinatal cystic kidney diseases have been published . The following recommendations are based on these published practice guidelines, additional data, and the authors' personal experience managing individuals with this disorder. Note: Because some data on ARPKD predates the understanding of its heterogeneous genetic causes, information in this section is based on both study cohorts with ARPKD in general and cohorts with ARPKD-PKHD1 .
To establish the extent of disease and needs in an individual diagnosed with ARPKD-PKHD1, the following evaluations are recommended (if not already performed as part of the evaluation that led to the diagnosis).
Perinatal and infantile presentation (prenatal to age 1 year)
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
Individuals with hypertension should avoid sympathomimetic agents. In general, unless the clinical situation warrants their use, avoid known nephrotoxic agents including nonsteroidal anti-inflammatory drugs (NSAIDs) and aminoglycosides. High-salt diet, smoking, and obesity should be avoided. Minimize use of potentially hepatotoxic agents (e.g., acetaminophen doses 30 mg/kg/day, herbal supplements, and alcohol). While work in cell and animal models suggests that caffeine, theophylline-like agents, and calcium channel blockers may exacerbate the formation and growth of renal cysts, this hypothesis has not been rigorously studied in individuals with ARPKD. Thus, the clinical relevance of these observations remains unclear.
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
Recent studies in two animal models of ARPKD suggest that tesevatinib (TSV), a unique multikinase inhibitor, markedly slows the progression of both renal cystic disease and hepatobiliary disease . These data, in addition to safety data generated by a Phase I/II multicenter clinical trial of TSV (also called KD-019) in ADPKD (NCT01559363), have led to an initial Phase I/II multicenter clinical trial of TSV in infants and children with ARPKD. To date, results have not been published. Two multinational open-label Phase III trials on the effects of tolvaptan in ARPKD-PKHD1 have been initiated . One trial focuses on children with a high risk for KRT in the first year of life based on recently established risk patterns for dialysis dependency.
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
View trials for polycystic kidney disease 4
To monitor existing manifestations in all individuals regardless of age of initial presentation, the individual's response to supportive care, and the emergence of new manifestations, the following evaluations are recommended.
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
Phenotype severity distribution: 2 very common features, 2 common features.
No clinical trials have been registered for polycystic kidney disease 4.
206 publications have been identified in PubMed for polycystic kidney disease 4. Kisho has analyzed 110 by research type. Research spans Review / Meta-Analysis (73%), Basic Science / Preclinical (11%), and Epidemiology / Natural History (7%).
Research Type | Count | % of Total |
|---|---|---|
Research summaries | 80 | 73% |
Laboratory research | 12 | 11% |
Disease patterns and progression | 8 | 7% |
Clinical study results | 4 | 4% |
Patient case studies | 2 | 2% |
New treatment approaches | 2 | 2% |
Other research | 1 | 1% |
Testing and diagnosis research | 1 | 1% |
Du K (2026). [PMID: 40882922](https://pubmed.ncbi.nlm.nih.gov/40882922/). *J Hepatol*. [Review / Meta-Analysis]
Ma D (2026). [PMID: 41653026](https://pubmed.ncbi.nlm.nih.gov/41653026/). *Genet Med*. [Diagnostic / Biomarker]
Heering G (2026). [PMID: 38477576](https://pubmed.ncbi.nlm.nih.gov/38477576/). *Cardiol Rev*. [Review / Meta-Analysis]
Álvarez-Vásquez JL (2026). [PMID: 41225097](https://pubmed.ncbi.nlm.nih.gov/41225097/). *Adv Exp Med Biol*. [Review / Meta-Analysis]
Franz A (2026). [PMID: 41314408](https://pubmed.ncbi.nlm.nih.gov/41314408/). *Semin Liver Dis*. [Review / Meta-Analysis]
Siddle M (2026). [PMID: 41214287](https://pubmed.ncbi.nlm.nih.gov/41214287/). *Nat Rev Gastroenterol Hepatol*. [Review / Meta-Analysis]
Kwak M (2025). [PMID: 39523478](https://pubmed.ncbi.nlm.nih.gov/39523478/). *Korean J Physiol Pharmacol*. [Basic Science / Preclinical]
Rahim MN (2025). [PMID: 39922676](https://pubmed.ncbi.nlm.nih.gov/39922676/). *Lancet*. [Review / Meta-Analysis]
Gibert-Ramos A (2025). [PMID: 39355871](https://pubmed.ncbi.nlm.nih.gov/39355871/). *Clin Mol Hepatol*. [Review / Meta-Analysis]
Hino K (2025). [PMID: 40965654](https://pubmed.ncbi.nlm.nih.gov/40965654/). *J Gastroenterol*. [Review / Meta-Analysis]
Data assembled from 6 of 12 sources · Last updated Nov 3, 2026, 11:14 AM UTC
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Online Mendelian Inheritance in Man
Genetic and Rare Diseases Info Center
Childhood (1 year)/ young adulthood |
|---|
Lung | Pulmonary hypoplasia | +/++ |
Kidney | Enlarged kidneys | +++ |
Chronic kidney disease | +++ | +++ |
Kidney failure | ++ | +/++ |
Liver | Hepatomegaly | +/++ |
Portal hypertension | (+) | + |
Splenomegaly | (+) | + |
Cholangitis | (+) | + |
Source: GeneReviews — "Autosomal Recessive Polycystic Kidney Disease–PKHD1"
AI-curated news mentioning polycystic kidney disease 4
Updated Oct 22, 2026
Investors are reassessing opportunities in kidney disease therapies, driven by new delivery strategies and regulatory clarity. ProKidney and Nephrogen's CEOs highlight the potential for commercially viable products in a historically challenging market.
A recent case report highlights the co-occurrence of aortic dissection and polycystic kidney disease, suggesting a potential link between these conditions. This discovery may prompt further research into their relationship and implications for patient management.
OMass’s molecule is vying to become an alternative to a Neurocrine Biosciences drug that is currently the only FDA-approved therapy for congenital adrenal hyperplasia. But Vertex Pharmaceuticals could also compete with a drug candidate from a recent acquisition. By Lisa Brooks, Vice President, Healthcare Partnerships · Here’s a recap of other recent life sciences financing activity: —Estuary Biotherapeutics launched, revealing $103 million in funding for two gene therapies in development for autosomal dominant polycystic kidney disease (ADPKD), an inherited progressive disorder that leads to the growth of cysts on the kidneys. An undisclosed private family fund and foundation led BrainChild’s Series A round. —Moonwalk Biosciences raised $70 million as it looks to bring obesity drug candidate MW101 into the clinic next year. The South San Francisco- and San Diego-based biotech develops small-interfering RNA that is delivered to adipose tissue to precisely modulate pathways that are different than the ones addressed by GLP-1 drugs. But Vertex Pharmaceuticals could also compete with a drug candidate from a recent acquisition. ... OMass Therapeutics now has $310 million in financing to support a pipeline led by a drug in development for a rare endocrine disorder with limited treatment options. The disease is congenital adrenal hyperplasia (CAH), an inherited condition in which patients lack an enzyme the adrenal glands need to produce key hormones. This drug came from Vertex’s recently closed $10 billion acquisition of Crinetics Pharmaceuticals. OMass’s new capital will support plans to bring OMS1620 through Phase 2 testing in CAH and ACTH-dependent Cushing’s syndrome. The Series C round announced on Oct. 15 will also support OMass’s earlier-stage assets. A drug the company describes as a potential first-in-class SLC15A4 inhibitor is in development for lupus and other diseases associated with interferon overproduction and pathogenic B-cell activation.
Estuary Biotherapeutics is seeking to address the root cause of autosomal dominant polycystic kidney disease with two gene therapy programs based on science from Yale.
Roche and Ionis Pharmaceuticals' RNA therapy, sefaxersen, demonstrated a reduction in protein levels in urine during late-stage testing, indicating potential improvements in kidney function. This progress may expedite FDA approval for the treatment of kidney disease.