Nephrons are the key working components of the kidney. Each nephron is composed of a renal corpuscle (glomerulus and Bowman's capsule) and a renal tubule. The glomerulus and Bowman’s capsule of the renal corpuscle is the basic filtration units of the kidney while the renal tubule performs many functions critical to multi-organ regulation and immunomodulation such as:

• Gluconeogenesis - generating glucose from non-carbohydrate substances.
• Ammoniagenesis – regulating acidity.
• Glutathione metabolism – regulating free radicals from exceeding the body's ability to neutralize and eliminate them.
• Breakdown (catabolism) of peptide hormones, growth factors and cytokines into smaller units to release energy or to use in anabolic reactions.

Kidney disease arises when nephrons are damaged. This leads to sudden and short-lived diseases (acute kidney failure) or slow and progressive diseases (chronic kidney disease).

Acute kidney failure - also called acute renal failure or acute kidney injury (AKI) - occurs when the kidneys suddenly become unable to filter waste products from blood. When kidneys lose their filtering ability, dangerous levels of waste accumulate and blood chemistry is unbalanced.

Diabetic nephropathy, also known as diabetic kidney disease, slowly progresses over the years. It is the chronic loss of kidney function occurring in those with poorly controlled diabetes mellitus. Due to damage to the glomeruli, protein loss in the urine may become massive and cause a low serum albumin. This results in generalized body swelling (oedema) and nephrotic syndrome. The estimated glomerular filtration rate (eGFR) may progressively fall as well. When the eGFR falls to 15ml/min/1.73m², the patient is diagnosed with end-stage kidney/renal disease (ESKD / ESRD).

Glomerulonephritis refers to an inflammation of the glomerulus. This inflammation typically results in nephrotic and/or nephritic syndromes. Nephrotic syndrome is characterised by oedema with increased protein in the urine (proteinuria), increased fat in the blood and decreased protein in the blood. Nephritic syndrome is characterised by blood in the urine (hematuria), decreased urine output and hypertension.

Chronic kidney disease (CKD) is most often caused by hypertension and/or diabetes. Hypertension increases the pressure on the glomeruli. Glomeruli are the tiny blood vessels in the kidneys where blood is cleaned. Over time, the increased pressure damages these vessels and kidney function begins to decline. With diabetes, increased blood sugar levels damage blood vessels in the kidneys thereby hindering their ability to clean blood efficiently and properly. Kidney failure occurs when the body becomes overloaded with toxins.

If left untreated, chronic kidney disease will eventually lead to kidney failure. Current treatments use hypertension and cholesterol medication such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) to preserve kidney function. When the kidneys have completely failed or are close to failing (ESKD / ESRD), patients are put on haemodialysis or peritoneal dialysis until a donor kidney is found. However, organ availability does not come close to meeting demand.

How Our Products Can Treat Kidney Diseases

We use products derived from human baby umbilical cords in all our therapy programs - Wharton's Jelly MSCs (wjMSCs). Our products are special because they can:

• reduce inflammation and oxidative stress ^[1,2].
• improve renal function ^[2,3,4].
• decrease serum urea nitrogen levels ^[2,3].
• decrease serum creatinine levels ^[2,3,5].
• increase creatinine clearance ^[2,5].
• decrease urinary proteins ^[5].
• reduce tubular injury score ^[2,3].
• increase renal tubular cell proliferation ^[3,4].
• reduce apoptotic events ^[3,4].
• reduce renal fibrosis ^[4,6].
• prevent rejection by regulating the immune system (immunomodulation) ^{[7,8,9,10,11,12,13]}.
• incapable of forming tumours ^{[7,8,14,15,16]}.

Treating Kidney Diseases

There are currently numerous clinical trials exploring the use of wjMSCs in the treatment of kidney diseases. These have been registered but results and findings have yet to be posted ^{[17,18,19,20]}.

In 2017, American researchers performed a clinical trial using 28 renovascular disease (RVD) patients. The intervention group (14 patients) received a single infusion of 100,000 or 250,000 of the patients’ own (autologous) adipose MSCs (aMSCs) per kilogram of body weight plus standardized medical treatment. 3 months after infusion, cortical perfusion and renal blood flow (RBF) rose in the post-stenotic kidney tissue (STK), contralateral kidney RBF increased and STK renal hypoxia decreased from 12.1% to 6.8% while single-kidney GFR remained stable ^[21].

In 2018, Iranian researchers published the findings of their 18-month study of 7 patients with CKD. They administered an intravenous infusion 1 to 2 million autologous bone marrow MSCs (bmMSCs) per kilogram of body weight. The primary endpoint was safety, which was measured by the number and severity of adverse events. Follow-up visits of all 7 patients did not observe any cell-related adverse events during the trial ^[22].

In 2019, a Chilean study intravenously infused 1 million autologous adipose MSCs (aMSCs) per kilogram of body weight into 6 CKD patients. Patients were stabilized and followed for 1 year prior to MSC infusion and 1 year following infusion. None patients presented with adverse effects. Patients experienced statistically significant improvement in urinary protein excretion; however, the glomerular filtration rate (GFR) was not significantly decreased ^[23].