Kidney Disorders

Kidney disease is any disorder that affects how the kidneys function. A list of all of the diseases and conditions that can affect kidney function and the possible causes are beyond the scope of this protocol. However, some of these disorders include analgesic nephropathy, chronic nephritis, diabetes, ESRD, hypertension, infection, injury, kidney stones, lupus erythematosus, and ADPKD (NORD 2002).

Symptoms of renal disease can include frequent headaches and urination, itching, poor appetite, fatigue, burning bladder, anemia, baggy eyes, nausea and vomiting, swollen or numb hands or feet, poor concentration, darkened skin, and muscle cramps (NORD 2002).

Kidney Stones (Calculi)

Kidney stones (or calculi) are a common and incredibly painful condition. It is estimated that 10% of the United States population will pass a kidney stone at some time in their lives. Men have more kidney stones than women, and white people are more prone to kidney stone formation than black people. The incidence of kidney stones is higher in the summer. This may be because people perspire more in the summer; as a result, urine becomes more concentrated.

A kidney stone is a solid, rock-like type of material that has formed or is present in the kidneys, ureters, or bladder. A kidney stone is formed from mineral substances that precipitate from urine. Kidney stones can stay in the kidney or travel down the urinary tract. Small stones are sometimes passed from the body with either a small or large degree of pain. Larger stones may lodge in the ureter, bladder, or urethra, blocking urine flow and causing extreme pain (NIDDK 1998).

Most kidney stones contain calcium combined with either oxalate or phosphate. Calcium stones are formed when extra calcium is not eliminated in the urine. Another type of kidney stone is a struvite stone, which can form following a urinary infection. Uric acid stones form when there is too much acid in the urine. A rare type of kidney stone is made up of cystine. Evidence shows that cystine-based stones tend to be inherited (the result of a genetic disease) (NIDDK 1998).

Kidney stones vary widely in size: from a grain of sand to the size of a golf ball. Although most kidney stones are quite small, they can grow to a size that is life threatening or requires surgical removal. Some large kidney stones, due to age of the patient or danger of associated trauma to a vital organ, cannot be surgically removed.

Kidney stones are usually yellow or brown in color. Their structure and texture can be smooth or jagged. Another common visual characteristic is a crystalline appearance with different mineral striations appearing throughout the structure of the stone. Examination and testing of a kidney stone by a urologist (ie, specialist in urology) can determine significant information about possible cause of the kidney stone, and perhaps suggest a remedy for individuals with potential to form additional kidney stones (NIDDK 1998).

As noted earlier, kidney stones tend to be inherited. They can also be associated with geographic factors. Therefore, people living in tropical climates may be at greater risk for kidney stone formation due to the way bodies manage water in a tropical setting. Perspiration often becomes the prevalent method of how the body excretes water in tropical or very hot conditions, and urination may decline slightly due to urine being stored longer in the urinary tract. Most people do not drink enough water; in tropical areas, this is even more significant. Excessive perspiration becomes more significant while engaging in physical labor or strenuous sports in hot conditions. The body loses large amounts of water during excessive perspiration. For example, a NFL lineman can lose up to a gallon of water (or up to 10 lbs of water weight) during a 4-hour game. Therefore, sufficient water intake is both a preventive and a therapeutic measure.

Symptoms of a kidney stone attack include sudden extreme pain in the lower back, side, or groin; blood in the urine; fever and chills; vomiting; a bad odor or cloudy appearance to the urine; and a burning sensation during urination. Any of these symptoms require evaluation by a physician. Pain in the lower back, side, or groin can also indicate that a kidney stone is moving or there is a serious urinary tract blockage that requires immediate medical intervention. Kidney stone episodes frequently include urinary tract infections (UTIs). Recurrent, untreated UTIs can eventually cause permanent kidney damage and reduced kidney function.

Passing a kidney stone can be as simple as drinking large amounts of liquid and running up and down stairs or jumping up and down vigorously to dislodge the stone. This practice uses the basic physics of gravity to get the stone moving so that it can be passed normally. If possible, catch the stone in a strainer or retrieve it to be examined by a nephrologist or urologist (NIDDK 1998).

Medical Intervention for Kidney Stones

Many kidney stones pass from the body naturally. However, more complex procedures are required to assist stones that cannot be passed or remove stones that are growing larger (NIDDK 1998). Either lithotripsy or surgical removal of the stone is used when a kidney stone is firmly lodged in the ureters, bladder, or urethra. In the past, these stones represented a significant health concern because the only way to remove them was invasive surgery with a high risk of postoperative infection. It is now possible for urologists to avoid surgery, except when there is no alternative. Newer methods to remove kidney stones include ureteroscopy, tunnel surgery, extracorporeal shock wave lithotripsy (ESWL), and percutaneous lithotripsy. These methods break the stone into smaller pieces so it can be removed or passed through the urinary tract (NIDDK 1998).

Preventing Kidney Stones

Research into the prevention of recurrent kidney stones has produced many helpful dietary guidelines, nutritional protocols, and lifestyle changes that can reduce or eliminate the potential for recurring kidney stones. They may also help pass a recurrent stone faster and with less difficulty.

In 1997, a double-blind study was conducted to determine if potassium/magnesium citrate would prevent recurrent formation of calcium oxalate kidney stones (Ettinger 1997). Sixty-four patients with a history of renal calculi were given 42 milliequivalents (mEq) potassium, 21 mEq magnesium, and 63 mEq citrate or a placebo daily for 3 years. New renal calculi formed in 63.6% of patients receiving placebo. Patients receiving potassium/magnesium citrate presented with 12.9% recurrent renal calculi. The study concluded that "potassium/magnesium citrate effectively prevents recurrent calcium oxalate stones, and this treatment given for up to 3 years reduces risk of recurrence by 85%" (Ettinger 1997).

Two major studies have shown that calcium should not be reduced for patients with a history of kidney stones (Takei 1998; Williams 2001). It was originally postulated that patients with a history of renal calculi should limit their calcium intake. Newer findings contradict this restriction and offer scientific evidence that uncombined intestinal oxalic acid is the real culprit for calcium oxalate kidney stones (Ohgitani 2000).

Harvard researchers studied nearly 92 000 nurses over a 12-year period to determine the relationship between calcium intake and occurrence of renal calculi (the well-known Harvard Nurses' Health Study). The study concluded that those nurses who consumed diets higher in calcium were at lower risk for kidney stones.

The reason this type of dietary modification reduced the chance of kidney stones was relatively simple. A high percentage of kidney stones are comprised of calcium and oxalic acid, which form calcium oxalate inside the kidneys. Oxalic acid is able to pass through the intestinal wall, into the blood, and enter the kidneys where it has a chance to combine with calcium. Calcium oxalate, when normally combined inside the digestive tract, does not pass through the intestinal wall and into the blood, but is eliminated with other waste products. Therefore, when combined with dietary or supplemental calcium inside the intestinal tract, oxalic acid will never reach the kidneys; thus, calcium oxalate kidney stones cannot be formed.

The Harvard Nurses' Health Study presented the following important findings: dietary calcium intake from food or supplements reduced the risk of renal calculi; calcium supplementation must be taken with food and in small dosages (< 400 mg); plant foods high in calcium, fiber, vitamins, minerals, antioxidants, and some protein were an excellent source of dietary phytochemicals.

Another study conducted in South Africa found that "mineral water containing calcium and magnesium deserves to be considered as a possible therapeutic or prophylactic agent in calcium oxalate kidney stone disease" (Rodgers 1997). A French mineral water containing 202 parts per million (ppm) calcium and 36 ppm magnesium was selected as the delivery method. Twenty males and females with previously formed calcium oxalate renal calculi and 20 healthy males and females participated in the study. Each subject provided daily 24-hour urine collection samples during the study. Mineral water was ingested over a 3-day period; then, participants switched to tap water. The cycle was repeated at least twice by each subject. Males with a history of calcium oxalate renal calculi received the most benefit, showing nine risk factors favorably affected by the mineral water containing calcium and magnesium (Rodgers 1997).

Recommendations to avoid kidney stones include (NKUDIC 1998):

• Drink more water. Try to drink at least 12 full glasses of water each day. Drinking extra water helps to flush substances that form stones from the kidneys.
• It is not necessary to eliminate coffee, tea, and colas from your diet, but limit caffeine because it can increase fluid loss. Consider drinking ginger ale, lemon-lime soda, and fruit juices.
• Follow your physician's recommendations about dietary limitations. If you form uric acid stones, your physician will probably ask you to eat less meat because meat breaks down to form uric acid.
• Follow your physician's recommendations about taking medicines to prevent kidney stone formation.

Auotosomal Dominant Polycystic Kidney Disease (ADPKD)

ADPKD is one of the most common genetic diseases in humans. It is a systemic disease caused by at least three different genes: PKD1, PKD2, and PKD3. However, most mutations are found in the PKD1 gene (Merta 1997; Sessa 1997). ADPKD is a very serious disease. Worldwide, it is responsible for 8-10% of all cases of ESRD. Patients with ADPKD develop cysts in both kidneys. These cysts continue to grow over the lifetime of the patient and ultimately lead to hypertension, reduced kidney function, and eventually renal failure. Poor kidney function in ADPKD patients accounts for many kidney transplants each year. According to the Polycystic Kidney Disease (PKD) Foundation (Kansas City, www.pkdcure.org), 60% of individuals with ADPKD develop kidney failure or ESRD. The only treatment is dialysis or transplant. Interestingly, because ADPKD is genetic in origin, persons who receive kidney transplants do not reacquire their genetic mutation with transplanted kidneys. Common symptoms are frequent infections, blood in the urine, and back pain.

Polycystic kidney disease (PKD) may occur at birth, during childhood or adulthood. Congenital polycystic disease can be detected at birth and may affect all or only small parts of one or both kidneys. Childhood PKD can cause death after a few years due to liver and kidney failure. In some adults, the disease may be present at birth, but not manifest any symptoms until young adulthood or middle age. In adults, it can affect either one or both kidneys (Glanze 1996). PKD is characterized by autonomous cellular proliferation, pockets of fluid accumulation within the cysts, and intraparenchymal fibrosis of the kidney. Other clinical observations include renal failure, liver cysts, and cardiac valve abnormalities (Bacallao 1997).

The traditional method of diagnosing ADPKD has been detecting renal cysts via ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) of the kidneys. The challenge in diagnosing ADPKD is to detect it in people with the defective gene, but who may not have symptoms or show any developed cysts. Newer methods of DNA testing can now identify individuals who carry the defective gene, but are not symptomatic. For example, every member of four Chinese families with a known history of ADPKD showed unique DNA patterns (Yuan 1997). DNA diagnostic testing methods have value for patients with existing ADPKD, as well as for presymptomatic patients.

ADPKD progresses to end-stage renal insufficiency before the age of 73 years in about 50% of affected patients (Grantham 1997). It remains a mystery as to why some patients are affected by numerous cysts that form inside the proximal and distal tubules, while others are spared. The formation of cysts begins in early childhood, affecting less than 1% of tubules as a consequence of mutated DNA. The risk factors associated with PKD include gender (males progress more quickly than females), race (black patients progress more rapidly than whites), and other contributing factors such as hypertension and proteinuria. These factors can aggravate and accelerate PKD through to end term (Grantham 1997).

Because hypertension (a common and serious factor of ADPKD) usually occurs early in the disease (ie, before renal function begins to decrease), Doppler ultrasonography has been used to assess renal vascular resistance (RVR) by measuring resistive and pulsatility indices. In a study of 42 patients with ADPKD and 65 control subjects, it was found that Doppler indices reflect increased RVR in those patients with ADPKD and that renal function disturbance did manifest systemic arterial hypertension (Brkljacic 1997). The abnormality of the kidneys in these patients was easily observed using ultrasound. However, this method did not show ADPKD potential for patients if renal cysts were not present. DNA testing is required to determine whether a patient carries the PDK1 and PDK2 chromosomes.

Cardiovascular complication is a very common cause of death for persons with ADPKD. After examining the relationship of known cardiovascular risk factors, hypertension, and ADPKD, researchers noted that left ventricular hypertrophy (LVH) is an important risk factor for premature cardiovascular death in persons with essential hypertension (Chapman 1997). Hypertension occurs frequently and early in ADPKD patients. In 116 adult ADPKD patients and 77 healthy controls, a higher frequency of LVH was found in ADPKD men (46% versus 20%) and women (37% versus 12%) compared to control subjects (Chapman 1997). LVH in ADKPD patients was associated with higher systolic and diastolic blood pressure. According to the researchers, the role of blood pressure as a contributing factor to LVH in ADPKD patients may be partly due to early onset and inadequate treatment.

The possibility is being explored that ADPKD may have an emerging infectious disease component as well. Research has shown fungal DNA in kidney tissue and cyst fluids of ADPKD patients, but not in healthy kidneys of persons without ADPKD (Miller-Hjelle 1997). In a differential activation protocol assay, researchers showed bacterial endotoxin and fungal beta-D-glucans in cyst fluids from human kidneys with PKD. Tissue and cyst fluids were examined for fungal components and the serological tests showed Fusarium, Aspergillus, and Candida antigens. Researchers concluded that "endotoxin and fungal components, sphingolipid biology in PKD, the structure of PKD gene products, infection, and integrity of gut function [will establish a mechanism] for microbial provocation of human cystic disease" (Miller–Hjelle 1997).
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