Before relinquishing a kidney, it's important to know what they do, how they function, and how a body changes if one is removed.

The simple version; Food, water, etc. that enters into the body is absorbed through mucus membranes, villi (small intestine), aveoli (lungs) etc. and eventually makes its way to the bloodstream. The kidneys' job is to filter the blood, reabsorbing what the body can use and discarding what it cannot. Kidneys also regulate blood pressure, calcium balance, and formation of red blood cells. (183)

Here is a page with a good basic explanation of the body's renal system.  

And here is an anatomical diagram of the renal and urinary system within the human body, parts labeled.

Consequences of Nephrectomy (kidney removal)

Nephrons are the filtering units of the kidney (see diagram below). When a kidney is removed, the living donor loses 50% of her/his nephrons. These nephrons are never regained.

Nephron quantity varies between individuals. It is well known, however, that low birth weight, defined as less than 5.5 pounds or 3500 grams, is highly correlated with a low nephron number (179). Some have suggested that those born with low birth weight should not be living kidney donors due to their lack of renal reserve, and increased risk of living with compromised kidney function. 

The generally accepted consensus is that when a kidney is donated, the remaining kidney 'grows' to compensate for the missing organ. The truth is a bit more complicated.

'Growth' is understood to signify the replication of cells to produce an overall larger organism. What occurs in the case of significant nephron loss (eg. a radical nephrectomy or kidney removal) is a swelling of the organ's individual cells, not an increase in their number.

Dr. Barry Brenner, the godfather, grandfather, and grand poobah of all things kidney-related (174), ascribes this change to an increase in the filtration rate of each individual nephron (25% of the body's blood is contained in the kidneys at all times. Donating a kidney means the remaining organ must handle the entire 25% rather than being split between the two organs.) This results from increased pressure within the kidney itself: a widening of the blood vessels, as well as greater plasma  pressure (the liquid part of the blood) as it pushes through the nephrons and glomerules. Consider what happens to a balloon when you blow into it.  

This process of increased SNGFR (single nephron glomerular filtration rate) is known as hyperfiltration, and the increased plasma pressure is known as glomeruler hypertension*.

The transplant industry promotes this renal compensation as an indicator of the safety of living kidney donation. However, hyperfiltration and glomeruler hypertension can also be a symptom of diabetes or kidney disease, and it can lead to glomerular damage(175) and other negative things (glomerules being the tiny pieces-parts of nephrons). How it can simultaneously be positive and yet a symptom is confusing to say the least.

Hypertension (aka High Blood Pressure)

Evidence exists that renal mass (ie. quantity of nephrons) is a major factor in the development of hypertension and glomerular injury. Transplant recipients have shown a reduction in blood pressure post-transplant (178), and living kidney donors have shown an increase in blood pressure post-donation (181).

Blood pressure increases as one ages, and renal function decreases. The younger the living donor, the greater the risk of developing life-threatening hypertension and/or kidney disease/failure (72).

(see Risks for more)

Proteinuria

Under normal conditions, protein molecules are too large to be filtered by the nephron's glomerules. However, under the pressure of hyperfiltration, these glomeruli can leak, allowing protein to be excreted in the urine.

 Microalbumin or albumin is a type of protein that can be detected by a urine test and is usually the first signal of glomeruli damage. Albuminuria is the hallmark of hyperfiltration damage. (173)

Protein levels in urine have been shown to a correlate with risk of death, cardiovascular event, end-stage renal disease and doubling of serum creatnine (204) independent of GFR (renal function).

Eating a low protein diet will ease the kidney's workload and help prevent this damage.

(Also see Kidney Diet and Risks for more)

The Sodium Situation

A reduction in nephrons limits the body's ability to secrete sodium, and causes sodium-sensitive hypertension.(180)

A 2012 CDC report states that 90% of Americans consume more sodium than recommended for a healthy diet. (214)

Bone Disease

Chronic Kidney Disease (GFR <60) is accompanied by disturbances in calcium, phosphate, vitamin D and parathyroid hormone levels that play an important role in the development and trajectory of renal bone disease (216). Increases in cardiac disease and death in patients with chronic kidney disease has been linked to these mineral abnormalities.

Creatinine

A waste product of protein and muscles. Measuring the level of creatinine to urea helps assess kidney function. As kidney disease progresses, the level of creatinine in the blood increases (dehydration can also cause a high creatinine level).

Normal ranges of creatinine are 0.3-0.7 mg/dL in children birth to three, 0.5-1.0 mg/dL in children 3-18 years old, and 0.6-1.3 mg/dL in adults (184)

*The term hypertrophy has also been used to describe this adaptation, but is more commonly associated with the muscles or heart. It is not seen as maladaptive in muscles, but can be a response to stress or disease in the heart. Hypertrophy is generally viewed as unfavorable or troublesome when seen in other organs, glands or body parts. 

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