Chronic Renal Disease in Two Canines With an IgA Deficiency

Posted on March 26th, 2015

Chronic renal failure may be a common occurrence with many various canine breeds or mixed breeds, based upon genetics or acquired through aging, stress, toxins in their environment, foods that contain pesticides (xenoestrogens) which are estrogen mimickers (including glyphosates), vegetables that contain plant estrogens (phytoestrogens) GMO foods, monthly insect chemicals, medical procedures, vaccinations, radiation, improper supplements, exercise, etc.

I would like to share with you two case studies that involve two canine patients with chronic renal failure.

Both patients were treated with the same standard therapy for the effects of chronic renal failure and yet their blood urea nitrogen (BUN) levels still remained very elevated.

The following tests were indicated and performed:

  • CBC and Blood Chemistry
  • Urinalysis
  • Urine Culture and Sensitivity
  • X-rays
  • Renal Biopsy
  • Ultrasound

The following treatments were recommended, depending on the veterinarian that was involved with the case:

  • Feeding a pure, low protein food
  • Multiple supplements
  • Homeopathic solutions
  • Chinese herbs
  • Acupuncture
  • Fluid therapy (Intravenous or subcutaneous)
  • Antibiotics
  • Steroids
  • Prescribing a phosphorus binder

Unfortunately, both canine patients did not respond to any of these traditional treatments that were indicated and that were definitely appropriate.

I was given the opportunity by the two different owners that did try all the various indicated treatments which still did not correct the chronic renal failure, to treat them.

The purpose of this article is to share with you these two case reports and suggest a possible alternative for an unresponsive renal failure patient that has an endocrine immune imbalance and does not respond to traditional renal therapy.


This case involves a neutered male, Chihuahua hybrid that is 4 years old.

The patient has a history of chronic renal failure for over two years. The owner was concerned that the day may come, when his chronic renal failure might reach such proportions that it would cause complete renal failure and death.

The owner was referred to me, and an endocrine immune blood test was performed.

The test results confirmed the fact that this patient has an endocrine imbalance which has caused a deficiency in IgA.

NOTE: IgA refers to the mucous membrane antibody that provides the protection for all mucous membranes in the body including the kidneys.

This patient had an IgA deficiency.

The following are the endocrine immune blood test results indicating the improvement that occurred with proper hormone supplementation and reregulation of his immune system.

Collection Date Total Estrogen Cortisol T3 T4 IgA IgG IgM
Units of Measure pg/mL ug/dL ng/dL ug/dL mg/dL mg/dL mg/dL
Low 20.00- 1.00- 100.00- 2.00- 70- 1000- 100-
High 25.00 2.50 200.00 4.50 170 2000 200
5/09/2014 25.17 3.36 93.42 1.81 53 741 73
6/13/2014 25.11 0.91 87.05 1.72 59 856 86
6/27/2014 25.10 0.94 85.67 1.6 60 874 87
7/18/2014 25.08 0.83 105.27 2.14 62 891 88
8/08/2014 25.05 0.81 134.64 4.18 65 932 92
8/29/2014 25.01 1.65 133.89 4.09 69 984 99
9/19/2014 24.99 2.15 128.68 3.51 71 1084 101
10/10/2014 24.97 1.51 130.17 3.6 75 1168 105
10/30/2014 24.99 0.98 125.64 2.84 71 1058 101
11/20/2014 24.98 1.02 107.52 2.45 73 1039 102
1/08/2015 25.01 4.43 107.09 2.41 69 1013 100
2/05/2015 24.97 1.81 103.68 2.12 73 1084 104
3/05/2015 24.97 1.07 106.93 2.55 73 1088 103

Once his immune system was protecting his kidneys, his elevated Blood Urea Nitrogen (BUN) returned to normal and has remained normal ever since.

The importance of IgA is that it provides protection for all the mucous membranes in the body.

It is produced by the B-lymphocytes which are regulated by the adrenal, hypothalamic-pituitary, thyroid axis.

It must be recognized that the endocrine system regulates the immune system.

Normally the immune system does not function on its own without being regulated by the endocrine system.

Once an IgA deficiency is identified, the impact areas of that deficiency are often dictated by the genetics of the patient and the patient’s parents.

What does this mean?

It means that when an IgA deficiency occurs, the impact area may affect many different areas and systems in the patient’s body. The site of the impact area many times is determined by gene inheritance (genetics).

The following systems may reflect these impact areas:

  1. The Respiratory System
    1. Chronic sneezing
    2. Chronic inflammation of the sclera (whites) of the eyes
    3. Reduced tear production
    4. Chronic nasal discharge
    5. Chronic coughing
    6. Chronic respiratory infections
    7. Asthma
    8. Post nasal drip
    9. Pulmonary infiltrates
    10. Cystic fibrosis
    11. Chronic pulmonary fibrosis
  2. The Digestive System
    1. Increased gastrointestinal sounds
    2. Excessive gas production
    3. Mucous envelop (a gelatinous cover surrounding the stool)
    4. Chronic vomiting
    5. Chronic diarrhea
    6. Increased gastrointestinal gas
    7. Acid reflux
    8. Ulcerative colitis
    9. Blood in the vomit or stool. NOTE: Please remember that the blood supply to the stomach and intestine in animals, is much closer to mucosal surface than in humans. Therefore, chronic vomiting and diarrhea may contain small amounts of blood. If the bleeding continues, please see your veterinarian.
    10. Increased thirst
    11. Increased urination
    12. Food allergies
    13. Chronic anal gland problems
    14. Pancreatitis with possible development of Diabetes Mellitus
    15. Irritable Bowel Syndrome
    16. Crohn’s diseases
  3. Urogenital System
    1. Chronic Bladder infections
    2. Chronic bladder inflammations. NOTE: Urine cultures and sensitivities may be negative and show no growth. NOTE: This chronic disease may be immune mediated and caused by an IgA deficiency.
    3. Chronic kidney disease
    4. Increase thirst
    5. Increased urination
    6. Certain types of urinary incontinence
    7. Bladder calculi (stones)
    8. Kidney calculi (stones)
  4. The Dermal (skin) System
    1. Chronic Inflammation of the skin of the abdomen
    2. Chronic licking of the paws
    3. Chronic ear infections
    4. Chronic ear inflammations
    5. Chronic eye inflammations
    6. Chronic itching of the face and nose
    7. Ear hematomas caused by excessive itching of the ear
  5. The Skeletal System
    1. Swollen joints
    2. Osteoarthritis
    3. Discospondylosis
    4. Rheumatoid arthritis
    5. Lumbosacral subluxations
    6. Easily ruptured ligaments (Anterior Cruciate ligament and Achilles’s tendon)
    7. Narrowed intervertebral disc spaces
    8. Panosteitis
    9. Nonspecific lameness

With this particular patient, his IgA deficiency was the cause of his chronic renal failure. However his IgA deficiency was developed due to his inactive or defective cortisol, which allowed for the production of an elevated adrenal estrogen.

NOTE: In a canine patient, if the IgA level is below 58 mg/dL, oral steroids will NOT be absorbed.

Since his IgA levels was below 58, it was necessary to bypass his gut with three long acting steroid injections, at 10 day intervals, until his adrenal estrogen decreased and his IgA level reached 58mg/dL.

When his adrenal estrogen level began to decrease, it allowed his B-Lymphocytes to function normally and produce higher levels of IgA, which would allow him to finally absorb oral steroids.

His thyroid hormones were not only deficient, but his elevated adrenal estrogen was binding the receptor sites for his body to use his thyroid hormones.

NOTE: The fact that an empirical or free hormone level falls within the normal range, will not indicate if that hormone can be used by the body without testing for the specific end products that the hormone regulates.

With proper supplements to reregulate his endocrine regulation of his immune system his kidneys are now protected by his B-lymphocytes and with their production of normal amounts of IgA, his Blood Urea Nitrogen (BUN) has returned to normal and remained normal.


This case study involves a 5 year old, neutered, male Chihuahua hybrid with chronic renal failure.

After a period of time of the pet owner trying to reduce a very elevated BUN in a fairly young dog, the owner was referred to me to do an endocrine immune panel.

Collection Date Total Estrogen Cortisol T3 T4 IgA IgG IgM
Units of Measure pg/mL ug/dL ng/dL ug/dL mg/dL mg/dL mg/dL
Low 20.00- 1.00- 100.00- 2.00- 70- 1000- 100-
High 25.00 2.50 200.00 4.50 170 2000 200
8/15/2014 25.21 6.44 214.38 6.67 49 682 68
9/12/2014 25.14 0.82 68.14 0.78 56 773 74
10/10/2014 25.10 1.34 73.04 0.91 60 857 84

The test results identify a very low IgA and inactive cortisol, which is causing his elevated adrenal estrogen.

Of interest, is the fact that both the patient’s T3 and T4 are elevated.

These elevated thyroid levels could have been misconstrued for a patient that has hyperthyroidism, which is not the case with this patient.

The reason why the T3 and T4 are elevated, is due to the elevated adrenal estrogen, which binds his receptor sites for his T3 and T4. This elevated adrenal estrogen binding of his thyroid receptor sites, has reduced the metabolism of both the liver and kidneys. When this metabolic hypothyroidism occurs, the liver will not breakdown his thyroid hormones in a 24 hour period, and the kidneys will not excrete the breakdown products in 24 hours, and therefore there will be a buildup and elevation of both the T3 and T4.

NOTE: A true case of hyperthyroidism would have elevated levels of both thyroid hormones (T3 and T4), and the cortisol, estrogen and IgA would all be normal.

After a series of long acting steroid injections that helped reduce his elevated adrenal estrogen, the patients T3 and T4 hormone levels were also decreased.

NOTE: Unfortunately the owner misread the directions on giving the oral steroid and thyroid supplement, which has now been corrected. That is why the October blood test results have not returned to normal even though the patients BUN had returned to normal. Now that the patient is taking proper hormone supplements, his next endocrine immune panel will definitely improve.

The increase in the patients IgA, etc. has protected his kidneys enough that his BUN remains normal and reduces his chances of developing permanent kidney damage.

The purpose of this article is to share with you that some chronic renal failures may occur from an endocrine immune imbalance.

This imbalance is caused by the production of inactive cortisol, and an excess production of adrenal estrogen, which has caused an IgA deficiency.

For more information on IgA, please go to The Importance of IgA, Townsend Letter for Physicians and Patients, November 2005.


Dr. AL Plechner