The aim of the medical treatment is to slow the progression of chronic kidney disease by reducing blood pressure and albumin levels. The current published guidelines define ideal BP of <130/80 mmHg for patients with hypertensive nephropathy; studies show that anything higher or lower than this can increase cardiovascular risk. According to the African American Study of Kidney Disease (AASK) trial, after an additional 5 years follow-up upon completion of the 10-year trial, up to 65% of the cohort had progressive nephropathy despite having controlled the mean systolic BP level <135 mmHg.

ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors and aldosterone antagonists, are pharmacological treatments that can be used to lower BP to target levels; hence reducing neuropathy and proteinuria progression. The management plan should be individualized based on the condition of the patients including comorbidities and previous medical history.

In addition, there are lifestyle changes that can be made. Weight reduction, exercise, reducing salt intake can be done to manage hypertensive nephropathy.

Aggressive treatment of high blood lipids is warranted. Low-protein, low-salt diet may result in slower progression of CKD and reduction in proteinuria as well as controlling symptoms of advanced CKD to delay dialysis start. Replacement of erythropoietin and calcitriol, two hormones processed by the kidney, is often necessary in people with advanced disease. Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin. A target hemoglobin level of 9–12 g/dL is recommended. The normalization of hemoglobin has not been found to be of benefit. It is unclear if androgens help with anemia. Phosphate binders are also used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease. Although the evidence for them is limited, phosphodiesterase-5 inhibitors and zinc show potential for helping men with sexual dysfunction.

At stage 5 CKD, renal replacement therapy is usually required, in the form of either dialysis or a transplant.

Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression. They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD. Furthermore, ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD. Aggressive blood pressure lowering decreases peoples risk of death.

Although the use of ACE inhibitors and ARBs represents the current standard of care for people with CKD, people progressively lose kidney function while on these medications, as seen in the IDNT and RENAL studies, which reported a decrease over time in estimated GFR (an accurate measure of CKD progression, as detailed in the K/DOQI guidelines) in people treated by these conventional methods.

In 2014, Japan was the first country in the world to approve a pharmacological treatment for ADPKD followed by Canada and Europe, which approved the drug tolvaptan for ADPKD patients in the beginning of 2015. Tolvaptan, an aquaretic drug, is a vasopressin receptor 2 (V2) antagonist. Pre-clinical studies had suggested that the molecule cAMP could be involved in the enlargement of ADPKD cysts, and studies on rodents confirmed the role of vasopressin in increasing the levels of cAMP in the kidney, which laid the basis for the conduction of clinical studies. Because data from the Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP) led by Mayo Clinic showed that total kidney volume (TKV) predicted the risk of developing renal insufficiency in patients with ADPKD, the TEMPO 3:4 trial, which enrolled patients from 129 sites worldwide from 2007 to 2009, evaluated TKV as a primary end-point to test the efficacy of tolvaptan in ADPKD patients. That study showed a significant decrease in the ratio of TKV increase and deterring of renal function decline in ADPKD patients after treatment with tolvaptan; however, because laboratory test results regarding liver function appeared elevated in a percentage of patients enrolled in that study, the approval of the drug was either delayed by regulatory agencies or, as in case of the US, altogether denied.

Currently, the only clinical/pharmacological treatment available for ADPKD consists in reducing the speed in gain of total kidney volume (TKV) with aquaretics (i.e. tolvaptan), which can alleviate pain while giving the patients a better quality of life for over a mean of 3 years. After this period, patients can restart gaining TKV at pre-treatment rates and may eventually have to go through dialysis and kidney transplant. Paliative treatment modalities involve symptomatic medications (non-opioid and opioid analgesics) for abdominal/retroperitoneal pain. Before the advent of aquaretic medication, the only option for analgesic-resistant pain were simple or complex surgical procedures (i.e. renal cyst aspiration, cyst decortication, renal denervation and nephrectomy), which can result in complications inherent to surgery.

The goals of treatment are to slow the progression of kidney damage and control related complications. The main treatment, once proteinuria is established, is ACE inhibitor medications, which usually reduce proteinuria levels and slow the progression of diabetic nephropathy. Other issues that are important in the management of this condition include control of high blood pressure and blood sugar levels (see diabetes management), as well as the reduction of dietary salt intake.

In terms of treatment/management for medullary cystic kidney disease, at present there are no specific therapies for this disease, and there are no specific diets known to slow progression of the disease. However, management for the symptoms can be dealt with as follows: erythropoietin is used to treat anemia, and growth hormone is used when growth becomes an issue. Additionally, a renal transplant may be needed at some point.

Finally, foods that contain potassium and phosphate must be reduced

The optimal treatment is prevention. Rigorous and continuous control of phosphate and calcium balance most probably will avoid the metabolic changes which may lead to calciphylaxis.

There is no specific treatment. Of the treatments that exist, none are internationally recognized as the standard of care. An acceptable treatment could include:

- Dialysis (the number of sessions may be increased)

- Intensive wound care

- Clot-dissolving agents (tissue plasminogen activator)

- Hyperbaric oxygen

- Maggot larval debridement

- Adequate pain control

- Correction of the underlying plasma calcium and phosphorus abnormalities (lowering the Ca x P product below 55 mg2/dL2)

- Sodium thiosulfate

- Avoiding (further) local tissue trauma (including avoiding all subcutaneous injections, and all not-absolutely-necessary infusions and transfusions)

- Urgent parathyroidectomy: The efficacy of this measure remains uncertain although calciphylaxis is associated with frank hyperparathyroidism. Urgent parathyroidectomy may benefit those patients who have uncontrollable plasma calcium and phosphorus concentrations despite dialysis. Also, cinacalcet can be used and may serve as an alternative to parathyroidectomy.

- Patients who receive kidney transplants also receive immunosuppression. Considering lowering the dose of or discontinuing the use of immunosuppressive drugs in people who have received kidney transplants and continue to have persistent or progressive calciphylactic skin lesions can contribute to an acceptable treatment of calciphylaxis.

- A group has reported plasma exchange effective and propose a serum marker and perhaps mediator (calciprotein particles)

The management of this condition can be done via-improvement of any electrolyte imbalance, as well as, hypertension and anemia treatment as the individuals condition warrants.

According to the United States Renal Data System (USRDS), hypertensive nephropathy accounts for more than one-third of patients on hemodialysis and the annual mortality rate for patients on hemodialysis is 23.3%.

Haemodialysis is recommended for patients who progress to end-stage kidney disease (ESKD) and hypertensive nephropathy is the second most common cause of ESKD after diabetes.

Patient prognosis is dependent on numerous factors including age, ethnicity, blood pressure and glomerular filtration rate. Changes in lifestyle factors, such as reduced salt intake and increased physical activity have been shown to improve outcomes but are insufficient without pharmacological treatment.

Often, aggressive treatment is unnecessary for people with MSK disease that does not cause any symptoms (asymptomatic). In such cases, treatment may consist of maintaining adequate fluid intake, with the goal of decreasing the risk of developing kidney stones (nephrolithiasis). Cases of recurrent kidney stone formation may warrant evaluation for possible underlying metabolic abnormalities.

In patients with low levels of citrate in the urine (hypocitraturia) and incomplete distal renal tubular acidosis, treatment with potassium citrate helps prevent the formation of new kidney stones. Urinary tract infections, when they occur, should also be treated.

Patients with the more rare form of MSK marked by chronic pain typically require pain management. Non-obstructing stones in MSK can be associated with significant and chronic pain even if they're not passing. The pain in this situation can be constant. It is not certain what causes this pain but researchers have proposed that the small numerous stones seen in MSK may cause obstruction of the small tubules and collecting ducts in the kidney which could lead to the pain. This pain can often be debilitating and treatment is challenging. Narcotic medication even with large quantities is sometimes not adequate. Some success with pain control has been reported using laser lithotripsy (called “ureteroscopic laser papillotomy”).

Unfortunately, response to treatment is not guaranteed. Also, the necrotic skin areas may get infected, and this then may lead to sepsis (i.e. infection of blood with bacteria; sepsis can be life-threatening) in some patients. Overall, the clinical prognosis remains poor.

As of today, no agreed-upon treatment of Dent's disease is known and no therapy has been formally accepted. Most treatment measures are supportive in nature:

- Thiazide diuretics (i.e. hydrochlorothiazide) have been used with success in reducing the calcium output in urine, but they are also known to cause hypokalemia.

- In rats with diabetes insipidus, thiazide diuretics inhibit the NaCl cotransporter in the renal distal convoluted tubule, leading indirectly to less water and solutes being delivered to the distal tubule. The impairment of Na transport in the distal convoluted tubule induces natriuresis and water loss, while increasing the reabsorption of calcium in this segment in a manner unrelated to sodium transport.

- Amiloride also increases distal tubular calcium reabsorption and has been used as a therapy for idiopathic hypercalciuria.

- A combination of 25 mg of chlorthalidone plus 5 mg of amiloride daily led to a substantial reduction in urine calcium in Dent's patients, but urine pH was "significantly higher in patients with Dent’s disease than in those with idiopathic hypercalciuria (P < 0.03), and supersaturation for uric acid was consequently lower (P < 0.03)."

- For patients with osteomalacia, vitamin D or derivatives have been employed, apparently with success.

- Some lab tests on mice with CLC-5-related tubular damage showed a high-citrate diet preserved kidney function and delayed progress of kidney disease.

Management of hematuria is aimed at treating secondary causes of hematuria. If hematuria is a result of a UTI, treatment with antibiotics is usually initiated and urine testing repeated after 6 weeks. If hematuria is secondary to a kidney stone, then management depends on the size of the kidney stone. If the stone is small enough, usually less than 1 cm, then conservative management with analgesics and fluid hydration may be sufficient, however stones that are too bid may require removal by a urologist. Another common cause of hematuria is benign enlargement of the prostate (BPH), treatment is aimed at reducing the size of the bladder with medications like finasteride and symptomatic management with drugs like terazonsin or tamsulosin.

For people with exercise induced hematuria, management is conservative and involves cessation of strenuous activities and keeping hydrated. If the cause of hematuria is a result of malignancy, treatment and management depends on the type and stage of cancer and can involve chemotherapy, radiation or surgical resection of the tumor or organ involved.

Treatment for renal osteodystrophy includes the following:

- calcium and/or native vitamin D supplementation

- restriction of dietary phosphate (especially inorganic phosphate contained in additives)

- phosphate binders such as calcium carbonate, calcium acetate, sevelamer hydrochloride or carbonate, lanthanum carbonate, sucroferric oxyhydroxide, ferric citrate among others

- active forms of vitamin D (calcitriol, alfacalcidol, paricalcitol, maxacalcitol, doxercalciferol, among others)

- cinacalcet

- renal transplantation

- haemodialysis five times a week is thought to be of benefit

- parathyroidectomy for symptomatic medication refractive end stage disease

Everolimus is FDA approved for the treatment of angiomyolipomas. Treatment should be considered for asymptomatic, growing AML measuring larger than 3 cm in diameter.

Angiomyolipoma do not normally require surgery unless there is life-threatening bleeding. Some centres may perform preventative selective embolisation of the angiomyolipoma if it is more than 4 cm in diameter, due to the risk of haemorrhage.

People with tuberous sclerosis are advised to have yearly renal scans, though it is possible that patients with very stable lesions could be monitored less frequently. The research in this area is lacking. Even if no angiomyolipoma is found, one can develop at any life stage. The angiomyolipoma can grow rapidly.

In tuberous sclerosis, typically many angiomyolipomas affecting each kidney. It is not uncommon for more than one intervention to be required during lifetime. Since kidney function may already be impaired (up to half the kidney may be lost before function loss is detectable), it is vital to preserve as much kidney as possible when removing any lesion. Large angiomyolipomas are treated by embolisation which reduces the risk of haemorrhage and can also shrink the lesion. A side effect of this treatment is postembolisation syndrome: severe pain and fever however this is easily managed and lasts only a few days.

A ruptured aneurysm in an angiomyolipoma leads to blood loss that must be stopped (though embolisation) and compensated for (through intravenous fluid replacement). Therefore, removal of the affected kidney (nephrectomy) is strongly discouraged though may occur if the emergency department is not knowledgeable about tuberous sclerosis.

Embolisation involves inserting a catheter along the blood vessels to the tumour. The blood vessels are then blocked, typically by injecting ethanol or inert particles. The procedure can be very painful, so analgesics are used. The destroyed kidney tissue often causes post-embolisation syndrome, which manifests as nausea, vomiting, fever and abdominal pain, and lasts a few days. Embolisation (in general) has an 8% rate of morbidity and a 2.5% rate of mortality, so is not considered lightly.

Patients with kidney loss should be monitored for hypertension (and treated for it if discovered) and avoid nephrotoxic drugs such as certain pain relievers and IV contrast agents. Such patients who are unable to communicate effectively (due to age or intellectual disability) are at risk of dehydration. Where multiple or large angiomyolipomas have caused chronic kidney disease, dialysis is required.

Robotic assisted partial nephrectomy has been proposed as a surgical treatment of a ruptured angiomyolipoma combining the advantages both of a kidney preservation procedure and the benefits of a minimal invasive procedure without compromising the safety of the patient.

The long-term use of lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, is known to cause nephropathy.

Nephropathy can be associated with some therapies used to treat cancer. The most common form of kidney disease in cancer patients is Acute Kidney Injury (AKI) which can usually be due to volume depletion from vomiting and diarrhea that occur following chemotherapy or occasionally due to kidney toxicities of chemotherapeutic agents. Kidney failure from break down of cancer cells, usually after chemotherapy, is unique to onconephrology. Several chemotherapeutic agents, for example Cisplatin, are associated with acute and chronic kidney injuries. Newer agents such as anti Vascular Endothelial Growth Factor (anti VEGF) are also associated with similar injuries, as well as proteinuria, hypertension and thrombotic microangiopathy.

Treatment varies with the type of vascular disease; in the case of renal artery disease, information from a meta-analysis indicated that balloon angioplasty results in improvement of diastolic blood pressure and a reduction in antihypertensive drug requirements. In the case of peripheral artery disease, preventing complications is important; without treatment, sores or gangrene (tissue death) may occur. Among the treatments are:

- Quitting smoking

- Lowering cholesterol

- Lower blood pressure

- Lower blood glucose

- Physical activity

Treatment of an episode of cholesterol emboli is generally symptomatic, i.e. it deals with the symptoms and complications but cannot reverse the phenomenon itself. In kidney failure resulting from cholesterol crystal emboli, statins (medication that reduces cholesterol levels) have been shown to halve the risk of requiring hemodialysis.

In addition to measures for chronic kidney disease (CKD) of any cause, there is evidence that ACE inhibitors can slow the deterioration of kidney function in Alport syndrome, delaying the need for dialysis or transplantation. The development of proteinuria has been recommended as an indication for commencing treatment.

Once kidney failure has developed, patients usually do well on dialysis or with a kidney transplant. Very rarely the Alport molecule in the donor kidney causes an aggressive immune response in the recipient, 'Alport post-transplant anti-GBM disease'.

Gene therapy has been frequently discussed, but delivering it to the podocytes in the glomerulus that normally produce the type IV collagen in the glomerular basement membrane is challenging.

Diabetic nephropathy in type 2 diabetes can be more difficult to predict because the onset of diabetes is not usually well established. Without intervention, 20-40 percent of patients with type 2 diabetes/microalbuminuria, will evolve to macroalbuminuria.

Diabetic nephropathy is the most common cause of end-stage kidney disease, which may require hemodialysis or even kidney transplantation. It is associated with an increased risk of death in general, particularly from cardiovascular disease.

Early and aggressive treatment is required to control the disorder. Diuretic medications help rid the body of excess fluid. ACE inhibitor medications (like Captopril and others) and non-steroidal anti-inflammatory drugs (like indomethacin) are used to slow the spilling of protein (albumin) in the urine. Antibiotics may be needed to control infections. Patients may also take iron supplements, potassium chloride, thyroxine and other vitamins to replenish what minerals the kidneys have leaked out.

Most patients will undergo regular and frequent albumin infusion (often daily) to replace what kidneys have lost. Infusions are performed via IV so a central venous catheter will need to be surgically inserted into patients chest or groin.

Dietary modifications may include the restriction of sodium and use of dietary supplements as appropriate for the nature and extent of malnutrition. Fluids may be restricted to help control swelling.

Many patients have a gastrostomy tube (g-tube) inserted for medication and/or feeds. Some patients develop oral aversions and will use the tube for all feeds. Other patients eat well and only use the tube for medicine or supplemental feeds. The tube is also useful for patients needing to drink large amounts of fluids around the time of transplant.

Patient will require removal of the kidneys (one at the time or both), dialysis, and ultimately a kidney transplant.

It is not known whether ACE inhibitors or other treatments affect hearing loss. For those with classic Alport syndrome, hearing aids are often required in teenage or young adult years.

Several classes of antihypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the usual blood pressure of the person before the hypertensive crisis. In most cases, the administration of intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect, is suitable (but in many cases not readily available). Besides, nitroprusside runs a risk of cyanide poisoning. Other intravenous agents like nitroglycerine, nicardipine, labetalol, fenoldopam or phentolamine can also be used, but all have a delayed onset of action (by several minutes) compared to sodium nitroprusside.

In addition, non-pharmacological treatment could be considered in cases of resistant malignant hypertension due to end stage kidney failure, such as surgical nephrectomy, laparoscopic nephrectomy, and renal artery embolization in cases of anesthesia risk.

It is also important that the blood pressure is lowered smoothly, not too abruptly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% (within minutes to 1 or 2 hours), and then toward a level of 160/100 mm Hg within a total of 2–6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.

The diagnosis of a hypertensive emergency is not based solely on an absolute level of blood pressure, but also on the typical blood pressure level of the patient before the hypertensive crisis occurs. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.