Primary Hyperoxaluria

New primary hyperoxaluria research, summarized each month in plain language.

2026 so far: In the months covered (January 2026 to September 2026), real-world reports added clearer early patterns after starting lumasiran and more detail on transplant timing, while late diagnosis and ongoing oxalate burden kept coming up as concerns. Read the 2026 review

We also cover clinical trials.

Yearly update

2026 so far

January–September
  • Early lumasiran response. Routine-care reports helped show what early responses can look like, including differences by age.
  • Transplant approaches. Reports described both kidney-only pathways that include RNAi treatment and combined liver-kidney transplant experiences.
  • Disease burden. The months covered included repeated reminders that PH can progress and can involve organs outside the kidneys.
  • Diagnosis pathways. One dataset suggested faster genetic confirmation, while other reports pointed to ongoing testing bottlenecks.
  • Future treatments. Cell and animal studies explored several ways to lower oxalate-related measures, but none provided human results.
New

September 2026

Monthly research update
  • Early oxalate change. Oxalate measures often fell soon after starting lumasiran.
  • Age and early response. Early lab response was more common in children.
  • Targeted AGXT testing. Focused AGXT testing found causes in many Moroccan patients.

August 2026

Monthly research update
  • Liver-kidney transplant. All four children had working liver and kidney grafts at follow-up.
  • Post-surgery problems. Infection, bleeding, and rejection were reported and treated.
  • Late PH1 diagnosis. After kidney-only transplant, oxalate crystals damaged the new kidney.
  • Body-wide oxalate. Case reports described oxalate buildup outside the kidneys, including bones.

July 2026

Monthly research update
  • Faster genetic diagnosis. Genetic confirmation was faster in France, especially in children.
  • Plasma oxalate access. Limited plasma oxalate testing often slowed evaluation in a survey.
  • Center-to-center differences. Use of RNAi medicines, dialysis, and transplants differed by center.
  • Late pediatric severity. In one registry, many children already had kidney failure at diagnosis.

June 2026

Monthly research update
  • Liver-kidney transplant. One case report noted stable kidney function and stopping dialysis.
  • Dental care after transplant. One report described dental implants without complications during follow-up.
  • Progression to kidney failure. Studies in adults and children showed frequent progression to kidney failure.
  • Early gene-editing work. Animal studies lowered oxalate, but this is not proven in people.

May 2026

Monthly research update
  • Kidney transplant with lumasiran. One report described a kidney-only transplant while continuing lumasiran, with early graft function reported as good.
  • Stones after transplant. The same report noted that kidney stones and oxalate crystal deposits can still occur in the transplanted kidney.
  • Rare heart deposits. Separate reports described uncommon heart involvement from oxalate deposits.

April 2026

Monthly research update
  • Childhood kidney signs. PH1 often starts in childhood with kidney stones or calcium deposits in the kidneys.
  • Urine pattern for PH3. In one infant, a specific urine-chemistry pattern pointed to PH3 and helped separate it from another metabolic condition discussed by the authors.
  • Lower AGT enzyme activity. In lab experiments, a small chemical change on the AGT enzyme sharply reduced its activity.
  • Gene therapy in PH1 mice. In a PH1 mouse model, liver-targeted gene therapy restored liver AGT and normalized urinary oxalate.

March 2026

Monthly research update
  • Blocking oxalate production. In a PH2 mouse study, the drug N‑propargylglycine (N‑PPG) lowered urine oxalate and was linked to less kidney injury.
  • Fewer kidney crystals. Treated PH2 mice had less calcium oxalate crystal buildup in the kidneys than untreated mice.
  • Gut-related high oxalate. A case report showed that gut malabsorption (for example from pancreatic disease) can raise oxalate and cause kidney crystal injury that can look like genetic primary hyperoxaluria.

February 2026

Monthly research update
  • Oxalate lowering before transplant (PH1). One PH1 case report described a large drop in serum oxalate after starting lumasiran before transplant.
  • Kidney-only transplant outcome (PH1). In the same report, a kidney-only transplant was followed by stable kidney function reported at 12 months.
  • Genetic confirmation in PH2. In children with PH2, 17 different GRHPR gene changes were reported (including newly described variants), showing how genetic testing helps confirm the diagnosis.

January 2026

Monthly research update
  • Single child case. After starting lumasiran, the report noted short-term stability.
  • Oral drug in mice. In PH1 mice, an oral compound lowered urine oxalate.
  • AGT activity boost. In cells, a nanobody increased activity of faulty AGT variants.

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