The treatment of branchio-oto-renal syndrome is done per each affected area (or organ). For example, a person with hearing problems should have appropriate supports and prompt attention for any inflammation of the ear.

A specialist should observe any kidney problems. Surgical repair may be needed depending on the degree of a defect or problem, whether a transplant or dialysis is needed.

There no standardized effective treatment strategies for the condition. Severe fatal respiratory failure can develop; long-term treatment with macrolides such as clarithromycin, erythromycin and azithromycin has been empirically applied for the treatment of primary ciliary dyskinesia in Japan, though controversial due to the effects of the medications.

There is no cure for Alström syndrome; however, there are treatment aims to reduce the symptoms and prevent further complications. Some of these treatment aims include:

- Corrective lenses: tinted lenses that help with the sensitivity from bright lights. The patients may have to adapt to reading in Braille, use adaptive equipment, mobility aids, and adaptive computing skills.

- Education: patients with Alström syndrome suffering from intellectual disabilities must have access to education. They must be able to receive free and appropriate education. Some Alström syndrome patients are educated in normal classrooms. Other patients have to take special education classes or attend to specialized schools that are prepared to teach children with disabilities. Staff members from schools have to consult with patient's parents or caregivers in order to design an education plan based on the child's needs. In addition, the school may document the progress of the child in order to confirm that the child's needs are being met.

- Hearing aids: the battery-operated devices are available in three styles: behind the ear, in the ear, and inside the ear canal. Behind the ear aims for mild-to-profound hearing loss. In the ear aims for mild to severe hearing loss. Lastly, the canal device is aimed for mild to moderately severe hearing loss. Patients that have severe hearing loss may benefit from a cochlear implant.

- Diet: an appropriate and healthy diet is necessary for individuals with Alström syndrome because it could potentially decreases chances of obesity or diabetes.

- Occupational therapy: the therapist helps the child learn skills to help him or her perform basic daily tasks like eating, getting dressed, and communicating with others.

- Physical Activity: exercising reduces chances of being obese and helping control blood sugar levels.

- Dialysis: helps restore filtering function. With hemodialysis, a patient's blood circulates into an external filter and clean. The filtered blood is then returned into the body. With peritoneal dialysis, fluid containing dextrose is introduced into the abdomen by a tube. The solution then absorbs the wastes into the body and is then removed.

- Transplantation: patients that endure a kidney failure may undergo a kidney transplantation.

- Surgery: if the patient endures severe scoliosis or kyphosis, surgery may be required.

Treatment for NPS varies depending on the symptoms observed.

- Perform screening for renal disease and glaucoma, surgery, intensive physiotherapy, or genetic counseling.

- ACE inhibitors are taken to treat proteinuria and hypertension in NPS patients.

- Dialysis and renal transplant.

- Physical therapy, bracing and analgesics for joint pain.

- Other surgery treatments such as patella realignment, joint replacement, and the cutting away of the head of radius.

Typically, treatment for this condition requires a team of specialists and surgery. Below are the treatments based on the symptom.

The different manifestations of Birt–Hogg–Dubé syndrome are controlled in different ways. The fibrofolliculomas can be removed surgically, through curettage, shave excision, skin resurfacing, or laser ablation; however, this is not a permanent solution as the tumors often recur. The renal and pulmonary symptoms are managed preventatively: CT scans, ultrasounds, or MRIs of the kidneys are recommended regularly, and family members are advised not to smoke. MRIs are the preferred method for surveillance of the kidneys in people with BHD because they do not carry the same risk of radiation complications as CT scans and are more sensitive than ultrasounds. Smokers with Birt–Hogg–Dubé have more severe pulmonary symptoms than non-smokers. Though nephrectomy is sometimes indicated, kidney tumors in cases of Birt–Hogg–Dubé are often removed without taking the whole kidney, in a procedure called partial nephrectomy. Knockout mouse studies have shown that administration of rapamycin may mitigate the effects of FLCN mutations on kidneys and improve renal cancer prognoses because of folliculin's interaction with the mTOR pathway.

The frequency is unknown, but the disease is considered to be very rare.

While there is no cure for BGS, symptoms can be treated as they arise. Surgery shortly after birth can repair craniosynostosis, as well as defects in the hand to create a functional grasp. There are risks associated with untreated craniosynostosis, therefore surgery is often needed to separate and reshape the bones. Since patients with a RECQL4 mutation may be at an increased risk of developing cancer, surveillance is recommended.

There is currently recruitment for a clinical trial at Boston's Children Hospital.

Treatment depends on the severity and symptoms. Treatments include:

- Endovascular stenting.

- Renal vein re-implantation.

- Gonadal vein embolization.

A 1998 review noted that life expectancy is usually normal, but that there have occasionally been reported neonatal deaths due to PCD. A 2016 longitudinal study followed 151 adults with PCD for a median of 7 years. Within that span, 7 persons died with a median age of 65.

When originally characterized by Giedion, there was a relatively high mortality rate due to untreated kidney failure (end stage renal disease - ESRD). The remarkable improvements in kidney transplantation have reduced the mortality of Conorenal Syndrome substantially if not eliminated it entirely. Most diagnosis of the disease occurs when children present with kidney failure – usually between the ages of 10 and 14. There are no known cures for the syndrome and management of the symptoms seems to be the typical approach.

Unfortunately, treatment for the anti-synthetase syndrome is limited, and usually involves immunosuppressive drugs such as glucocorticoids. For patients with pulmonary involvement, the most serious complication of this syndrome is pulmonary fibrosis and subsequent pulmonary hypertension.

Additional treatment with azathioprine and/or methotrexate may be required in advanced cases.

Prognosis is largely determined by the extent of pulmonary damage.

Conorenal syndrome, also called Mainzer-Saldino syndrome or Saldino-Mainzer disease, is a collection of medical conditions that seem to have a common genetic cause.

A thorough diagnosis should be performed on every affected individual, and siblings should be studied for deafness, parathyroid and renal disease. The syndrome should be considered in infants who have been diagnosed prenatally with a chromosome 10p defect, and those who have been diagnosed with well defined phenotypes of urinary tract abnormalities. Management consists of treating the clinical abnormalities at the time of presentation. Prognosis depends on the severity of the kidney disease.

Prevention for Alström Syndrome is considered to be harder compared to other diseases/syndromes because it is an inherited condition. However, there are other options that are available for parents with a family history of Alström Syndrome. Genetic testing and counseling are available where individuals are able to meet with a genetic counselor to discuss risks of having the children with the disease. The genetic counselor may also help determine whether individuals carry the defective ALSM1 gene before the individuals conceive a child. Some of the tests the genetic counselors perform include chorionic villus sampling (CVS), Preimplantation genetic diagnosis (PGD), and amniocentesis. With PGD, the embryos are tested for the ALSM1 gene and only the embryos that are not affected may be chosen for implantation via in vitro fertilization.

Surgery to remove the clot is possible, but rarely performed. In the past, surgical removal of the renal vein clot was the primary treatment but it is very invasive and many complications can occur. In the past decades, treatment has shifted its focus from surgical intervention to medical treatments that include intravenous and oral anticoagulants. The use of anticoagulants may improve renal function in RVT cases by removing the clot in the vein and preventing further clots from occurring. Patients already suffering from nephrotic syndrome may not need to take anticoagulants. In this case, patients should keep an eye out and maintain reduced level of proteinuria by reducing salt and excess protein, and intaking diuretics and statins. Depending on the severity of RVT, patients may be on anticoagulants from a year up to a lifetime. As long as the albumen levels in the bloodstream are below 2.5g/L, it is recommended that RVT patients continue taking anticoagulants. Main anticoagulants that can be used to treat RVT include warfarin and low molecular weight heparin. Heparin has become very popular, because of its low risk of complications, its availability and because it can easily be administered. Warfarin is known to interact with many other drugs, so careful monitoring is required. If a nephrotic syndrome patient experiences any of the RVT symptoms (flank or back pain, blood in the urine or decreased renal function), he or she should immediately see a doctor to avoid further complications.

The main side effect of anticoagulants is the risk of excessive bleeding. Other side effects include: blood in the urine or feces, severe bruising, prolonged nosebleeds (lasting longer than 10 minutes), bleeding gum, blood in your vomit or coughing up blood, unusual headaches, sudden severe back pain, difficulty breathing or chest pain, in women, heavy or increased bleeding during the period, or any other bleeding from the vagina. Warfarin can cause rashes, diarrhea, nausea (feeling sick) or vomiting, and hair loss. Heparin can cause hair loss (alopecia) thrombocytopenia – a sudden drop in the number of platelets in the blood.

It has been reported in a case study of 27 patients with nephrotic syndrome caused RVT, there was a 40% mortality rate, mostly due to hemorrhagic complications and sepsis. In 75% of the remaining surviving patients, the RVT was resolved and renal function returned to normal. It has been concluded that age is not a factor on the survival of RVT patients, although older patient (55 and older) are more likely to develop renal failure. Heparin is crucial in returning normal renal function; in patients that did not take heparin, long term renal damage was observed in 100%. In patients that did take heparin, renal damage was observed in about 33%. By quickly treating, and receiving the correct medications, patients should increase their chances of survival and reduce the risk of the renal vein clot from migrating to another part of the body.

Surgery is an option to correct some of the morphological changes made by Liebenberg Syndrome. Cases exist where surgery is performed to correct radial deviations and flexion deformities in the wrist. A surgery called a carpectomy has been performed on a patient whereby a surgeon removes the proximal row of the carpal bones. This procedure removes some of the carpal bones to create a more regular wrist function than is observed in people with this condition.

Inborn errors of renal tubular transport are metabolic disorders which lead to impairment in the ability of solutes, such as salts or amino acids, to be transported across the brush border of the renal tubule. This results in disruptions of renal reabsorption.

Examples of these disorders include Iminoglycinuria, renal tubular acidosis and Gitelman syndrome.

Abderhalden–Kaufmann–Lignac syndrome (AKL syndrome), also called Abderhalden–Lignac–Kaufmann disease or nephropathic cystinosis, is an autosomal recessive renal disorder of childhood comprising cystinosis and renal rickets.

This is much more common, but is not usually of any major health consequence, as long as the other kidney is healthy.

It may be associated with an increased incidence of Müllerian duct abnormalities, which are abnormalities of the development of the female reproductive tract and can be a cause of infertility, blocked menstrual flow (hematocolpos), increased need for Caesarean sections, or other problems. Herlyn-Werner-Wunderlich syndrome is one such syndrome in which unilaterial renal agenesis is combined with a blind hemivagina and uterus didelphys. Up to 40% of women with a urogenital tract anomaly also have an associated renal tract anomaly.

Adults with unilateral renal agenesis have considerably higher chances of hypertension (high blood pressure). People with this condition are advised to approach contact sports with caution.

The odds of a person being born with unilateral renal agenesis are approximately 1 in 750.

The goals of surgical treatment are: reducing length of the thumb, creating a good functioning, a stable and non deviated joint and improving the position of the thumb if necessary. Hereby improving function of the hand and thumb.

In general the surgical treatment is done for improvement of the thumb function. However, an extra advantage of the surgery is the improvement in appearance of the thumb. In the past, surgical treatment of the triphalangeal thumb was not indicated, but now it is generally agreed that operative treatment improves function and appearance. Because an operation was not indicated in the past, there’s still a population with an untreated triphalangeal thumb. The majority of this population doesn’t want surgery, because the daily functioning of the hand is good. The main obstacle for the untreated patients might not be the diminished function, but the appearance of the triphalangeal thumb.

The timing of surgery differs between Wood and Buck-Gramcko. Wood advises operation between the age of six months and two years, while Buck-Gramcko advises to operate for all indications before the age of six years.

- For TPT types I and II of the Buck-Gramcko classification, the surgical treatment typically consists of removing the extra phalanx and reconstructing the ulnar collateral ligament and the radial collateral ligament if necessary.

- For type III of Buck-Gramcko classification proposable surgical treatments:

- For type IV of Buck-Gramcko classification the surgical treatment typically consists of an osteotomy which reduces the middle phalanx and arthrodesis of the DIP. This gives a shortening of 1 to 1.5 cm. In most cases, this technique is combined with a shortening, rotation and palmar abduction osteotomy at metacarpal level to correct for position and length of the thumb. The extensor tendons and the intrinsic muscles are shortened as well.

- For type V of the Buck-Gramcko classification the surgical treatment proposably consists of a "pollicization". With a pollicization the malpositioned thumb is repositioned, rotated and shortened, the above-described rotation reduction osteotomy of the first metacarpal can be performed as well.

- For type VI of the Buck-Gramcko classification, the surgical treatment typically consists of removing the additional mostly hypoplastic thumb(s). Further procedures of reconstruction of the triphalangeal thumb are performed according to the shape of the extra phalanx as described above.

Diagnosis depends on the clinical scenario. However, karyotyping is an essential test for diagnosis.

Affected children are developmentally delayed with dwarfism, rickets and osteoporosis. Renal tubular disease is usually present causing aminoaciduria, glycosuria and hypokalemia.

Cysteine deposition is most evident in the conjunctiva and cornea.

Renal agenesis is a medical condition in which one (unilateral) or both (bilateral) fetal kidneys fail to develop.

Unilateral and Bilateral Renal Agenesis in humans, mice and zebra fish has been linked to mutations in the gene GREB1L. It has also been associated with mutations in the genes "RET" or "UPK3A". in humans (see Rosenblum et al 2017 for review) and mice respectively.