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Kidneys, kidney disease and protein 
Most people have two bean-shaped kidneys, each about the size of a clenched fist, in the rear left and right sides of their torso, just below their ribs. They have many essential functions (e.g., regulating blood pressure, producing hormones and activating vitamin D), but most importantly they filter our blood and remove excess body fluids and wastes for elimination in the urine. They are able to balance out body fluid, electrolyte (salts) and acid (pH) levels so that all of our organs function optimally, despite our consumption of a variety of fluids from foods and beverages, and fluid losses from physical activity and sweating. Here’s how they do it.

Kidney function
Blood flows from the aorta (the main blood vessel from the heart) into the kidneys via the renal artery. Within the kidney, the parts that filter the blood are called nephrons. Within each nephron is a glomerulus, a bulb-like capsule which contains tiny blood vessels that look a bit like a loosely wound ball of wool.

When the kidney is functioning normally, these tiny blood vessels have a large number of fine holes. They work a bit like sieves, allowing water, some salts (e.g., sodium, potassium, calcium, phosphorus) and waste products to pass through, but they are too small to allow red and white blood cells, and most blood proteins, to leak out. The exact composition of the filtered fluids (filtrate) depends on the body’s requirements for essential minerals like sodium and potassium, the acid-base balance (pH), and concentration of wastes from general metabolism.

Eventually, the filtrate from each nephron flows together and enters collecting ducts within the kidney, where the concentration of the final urine product is determined. The urine then travels through the ureters to the urinary bladder for temporary storage before voluntary urination.

Kidney function is evaluated based on the glomerular filtration rate (the rate at which the kidneys form filtrate) and the amount of the protein albumin lost in the urine. In health, glomerular filtration rates are greater than 90mL/minute, and there is essentially no albumin in the urine.

Nephrotic syndrome occurs when the glomeruli are damaged, increasing the size of the filtration holes, and therefore decreasing their ability to prevent proteins (e.g., albumin, lipoproteins, clotting factors and immunoglobulins) from escaping into the urine. The loss of these proteins can lead to serious health problems including oedema, high cholesterol levels, blood clotting and immune issues. Nephrotic syndrome can be caused by infections, immune disorders, chemical damage (from medications or illicit drugs), or poorly managed diabetes.

Chronic kidney disease is characterised by gradual, irreversible deterioration of the nephrons. Because we have a lot of nephrons, chronic kidney disease develops over many years without causing any symptoms. People are therefore often diagnosed late in the course of the illness, after most kidney function has been lost. Like the nephrotic syndrome, damage to the blood vessels in the nephrons leads to excessive loss of proteins in the urine, which can lead to serious health problems including oedema, high cholesterol, blood clotting and immune issues. Additionally, the nephrons lose their ability to maintain electrolyte (e.g., sodium and potassium) levels, acid-base balance (e.g., uric acid and phosphorus levels) and uraemia (the level of urea – the waste product of protein metabolism – in the blood). The more common causes of chronic kidney disease include diabetes and hypertension (chronically high blood pressure).

The Recommended Dietary Intake (RDI) of protein for women is 0.75 g per kg body weight, and for men it is 0.84g per kg. High protein diets provide more than 1.2g per kg body weight and lower protein diets less than 0.6 g per kg body weight.

Unlike carbohydrate which is stored as glycogen in our muscles and liver, and fat which is stored as triglycerides in our fat cells, we have a limited capacity to store protein. If we eat more protein than our body’s require, some of it can be converted to glucose in the process of gluconeogenesis (see July 2019 edition of GI News). The metabolic process of converting proteins (or more specifically amino acids – the building blocks of proteins) to glucose leads to the production of ammonia, which in turn is converted to urea and excreted in the urine.

High protein diets increase glomerular filtration rates, which increases the pressure within the glomerulus and may cause damage in susceptible people. High protein diets also increase urea production. On the other hand, lower protein diets decrease the pressure within the glomerulus and produce less urea.

The highest quality evidence available to date suggests that high protein diets do not have a negative effect on the glomerulus in people with healthy kidneys as the glomerulus is able to cope with the increased pressure and higher urea content.

However, in people with nephropathy/chronic kidney disease, the increased glomerular pressure caused by a high protein diet may lead to increased protein (e.g., albumin) loss in the urine and consequently increase the rate of progression of kidney disease. Therefore, a lower protein diet of 0.6–0.8 per kg body weight is generally recommended to people with existing nephropathy/chronic kidney disease. The problem is, chronic kidney disease develops over many years without causing any symptoms, so some high-risk people (e.g., people with diabetes) may have the condition but not know it.

Finally, for people with nephropathy/chronic kidney disease, approximately half of the proteins should come from plant sources (e.g., beans, lentils, chickpeas, etc…), as there is some evidence that they place less stress on the kidneys than animal sources.

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Dr Alan Barclay
Alan Barclay, PhD is a consultant dietitian and chef (Cert III). He worked for Diabetes Australia (NSW) from 1998–2014 . He is author/co-author of more than 30 scientific publications, and author/co-author of  The good Carbs Cookbook (Murdoch Books), Reversing Diabetes (Murdoch Books), The Low GI Diet: Managing Type 2 Diabetes (Hachette Australia) and The Ultimate Guide to Sugars and Sweeteners (The Experiment, New York).

Contact: You can follow him on Twitter or check out his website.