The Airik Lab for the Investigation of Causes of Chronic Kidney Disease

Developing an Improved Understanding of Cellular and Molecular Mechanisms

The laboratory of Rannar Airik, PhD focuses on identifying the genetic and molecular mechanisms of chronic kidney disease including renal ciliopathies that may be targetable by therapy. To achieve this, the lab combines transgenic animal models and biochemical assays that provide a basis for further molecular dissection of the mechanisms involved in these human diseases.

Areas of Focus

Chronic Kidney Disease

Chronic kidney disease is a devastating condition that affects an increasing number of people in the world. It leads to a progressive loss of kidney function in affected individuals and ultimately necessitates dialysis or kidney transplantation for survival. The Airik Lab has demonstrated that impairment of DNA damage response in the kidney tubular epithelium can lead to kidney tubular injury and precipitate progressive fibrotic changes in the kidney, culminating in loss of kidney function. Investigating the role of DNA damage response in normal tubular maintenance and assessing how its deficiency underpins chronic kidney pathology is a high priority of our work.

Chronic Kidney Disease

MCM6 gene expression (orange) in karyomegalic tubular cells.

Renal Ciliopathies

Renal ciliopathies are a group of fibrocystic kidney diseases that are caused by structural or functional defects in the primary cilium, a whip-like cell-surface organelle, that regulates the activity of several cellular signaling pathways. Accordingly, mutations in ciliary genes, such as those encoding nephrocystins and nephronophthisis (NPHP) proteins, compromise the cilium and result in fibrocystic kidney pathology. Although, being a major genetic cause of childhood end-stage kidney disease, the pathomechanisms underlying NPHP are not well understood. To get better insights into the disease mechanisms and to develop therapies against this condition, we use transgenic animal models and cell culture systems.

Lab Team & Contact Information

Rannar Airik, PhD

Principal Investigator
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Merlin Airik, PhD
Post-doctoral Fellow

Amy B. Huynh
Research Technician

Contact Us

The Airik Lab
UPMC Children’s Hospital of Pittsburgh
John G. Rangos Sr. Research Center
4401 Penn Avenue
Pittsburgh, PA 15224


Primary coenzyme Q10 nephropathy, a potentially treatable form of steroid-resistant nephrotic syndrome
Tan W, Airik R
Pediatric Nephrology
2021 Jan 22

Roscovitine Blocks Collecting Duct Cyst Growth in Cep164-deficient Kidneys
Airik R, Airik M, Schueler M, Bates CM, Hildebrandt F
Kidney International
2019 Aug

Delayed Onset of Smooth Muscle Cell Differentiation Leads to Hydroureter Formation in Mice with Conditional Loss of the Zinc Finger Transcription Factor Gene Gata2 in the Ureteric Mesenchyme
Weiss AC, Bohnenpoll T, Kurz J, Blank P, Airik R, Lüdtke TH, Kleppa MJ, Deuper L, Kaiser M, Mamo TM, Costa R, von Hahn T, Trowe MO, Kispert A
The Journal of Pathology
2019 Mar 27

Treatment with 2,4-Dihydroxybenzoic Acid Prevents FSGS Progression and Renal Fibrosis in Podocyte-Specific Coq6 Knockout Mice
Widmeier E, Airik M, Hugo H, Schapiro D, Wedel J, Ghosh CC, Nakayama M, Schneider R, Awad AM, Nag A, Cho J, Schueler M, Clarke CF, Airik R, Hildebrandt F
Journal of the American Society of Nephrology
2019 Feb 8

Osteoclast Stimulation Factor 1 (Ostf1) KNOCKOUT Increases Trabecular Bone Mass in Mice
Vermeren M, Lyraki R, Wani S, Airik R, Albagha O, Mort R, Hildebrandt F, Hurd T
Mammalian Genome
2017 Dec

SDCCAG8 Interacts with RAB Effector Proteins RABEP2 and ERC1 and Is Required for Hedgehog Signaling
Airik R, Schueler M, Airik M, Cho J, Ulanowicz KA, Porath JD, Hurd TW, Bekker-Jensen S, Schrøder JM, Andersen JS, Hildebrandt F
PLoS One
2016 May 25

Opportunities to Join

We’d Like to Hear From You!

The Airik Lab is always welcoming applications from enthusiastic students or post-docs looking to work with us. For more information, please contact Dr. Airik via email.