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Clinical nephrology is the study of kidney diseases. We diagnose patients with a variety of kidney related diseases, and also manage them. Many of the diseases we deal with are secondary to hypertension or diabetes. We strive to prevent the progression of chronic kidney disease. An excellent resource about chronic kidney disease can be reviewed at MedlinePlus


Chronic kidney disease is a disorder that occurs when the kidneys do not function properly. The kidneys handle waste and fluids, help control the blood pressure, and keep many of the minerals and electrolytes (minerals with an electrical charge) in balance. They also activate hormones such as vitamin D, and make another hormone, erythropoietin, that is important in anemia.


As we age, kidney function normally becomes reduced, but it is very rare for persons, even with moderately advanced kidney disease, to require renal replacement therapy.


At Kidney Associates, our primary objectives are to prevent patients who have been diagnosed with chronic kidney disease from progressing. Also, we want to prevent the complications and other conditions that are associated with kidney disease from interfering with your life.


In some situations the kidneys will fail and renal replacement therapy will be necessary. If this happens, we want to assure that you will be able to select the modality of therapy that best fits your lifestyle, that you start kidney therapy in the best condition possible, and that you remain as healthy as you can during the course of your therapy.


Kidney Associates physicians work as consultants, and care for patients in one of the local Houston hospitals with a variety of kidney disorders. Acute kidney injury (AKI) is a condition that arises when the kidney function decreases over a few hours or days. It can occur in patients who are in the intensive care unit, and may occur after surgery, or in those who are elderly or very ill. Acute kidney injury is discussed in more detail below and on the National Kidney Foundation Website.


Dialysis is among the renal replacement therapies that some patients require when their kidneys fail. Although nearly one in nine patients have chronic kidney disease (CKD) only a very few actually require renal replacement therapy.


At Kidney Associates our goal is to prevent or delay the progression of kidney disease, but when it becomes so advanced that replacement therapy is needed, we optimally encourage a kidney transplant. Some patients undergo a transplant early and never require dialysis therapy.


If dialysis needed, our first choice is home dialysis – either peritoneal dialysis (performed through a catheter in the abdomen) or home hemodialysis (that you can do with a partner at your home).


For some patients, in center hemodialysis is the preferred option. This is staff assisted and can be performed during the day, or at night (nocturnal dialysis)


Many Kidney Associates physicians work as consultants in local Houston hospitals, and care for patients with a variety of kidney disorders. We see patients with chronic kidney disease and with acute kidney Injury. Often we see patients with congestive heart failure, or for acute disorders in fluid, electrolyte or acid-base balance. Many of the patients we will see are in the intensive care unit or are being managed in relation to surgery.


When kidneys no longer function, patient have either the choice of dialysis or a kidney transplantation. If you are eligible for a kidney transplant, your doctor will refer you to a kidney transplant center for further evaluation. Patients may either receive a transplant from a living donor or a deceased donor. Living donors may be relatives or friends. The potential donor must match, and also be healthy. In some situations, a kidney paired donation may be necessary. When a suitable living donor is not available, you may be placed on a transplant list to receive a deceased donor kidney. More information about kidney transplantation can be found from The United Network for Organ Sharing (UNOS).


Management strategies must be focused on the individual patient, and should start early to prevent disease progression. The major approach is to treat the underlying disease, control the blood pressure, use converting enzyme inhibitors (CEI) or angiotensin receptor blocker (ARB) therapy when possible, control metabolic acidosis, avoid toxic medications and focus on lifestyle modification.

Lifestyle modifications include dietary restriction (salt, sugar, protein phosphorus, uric acid and fat), the judicious use of vitamins, cigarette smoking cessation and exercise.

Source: Essentials of Chronic Kidney disease, SZ Fadem, Editor, Nova Biomedical, New York, 2018.


The glomerular filtration rate measures the rate that waste products are filtered through the glomerulus (kidney filter), and is a generally a valid index of kidney function.


The estimated glomerular filtration rate is a routine part of medical practice. It was derived from four variables (age, race, gender and serum creatinine) and developed in 1999. It is based on data obtained from the 1628 patients in the MDRD clinical trial, and compares the GFR with the urinary clearance of iothalamate.


It has evolved over the years, and the most current equation is the CKD-EPI 2012, taken from a diverse population of 5,352 patients. It again uses the urinary clearance of iothalamate as the standard.




Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate
method to estimate glomerular filtration rate from serum creatinine: a new
prediction equation. Modification of Diet in Renal Disease Study Group. Ann
Intern Med. 1999 Mar 16;130(6):461-70. PubMed PMID: 10075613.


Inker LA, Eckfeldt J, Levey AS, Leiendecker-Foster C, Rynders G, Manzi J,
Waheed S, Coresh J. Expressing the CKD-EPI (Chronic Kidney Disease Epidemiology
Collaboration) cystatin C equations for estimating GFR with standardized serum
cystatin C values. Am J Kidney Dis. 2011 Oct;58(4):682-4. doi:
10.1053/j.ajkd.2011.05.019. Epub 2011 Aug 19. PubMed PMID: 21855190; PubMed
Central PMCID: PMC4421875.




The diagnosis of chronic kidney disease is made by measuring a blood test known as the serum creatinine. Using age, race and gender, the estimated glomerular filtration rate (eGFR) can then be calculated. A popular website containing this equation is Once the eGFR is calculated, it can be used to diagnose and stage chronic kidney disease (CKD). There are 5 stages. CKD can be diagnosed when the eGFR is below 60 ml/min/1.73m2 for at least three months. The diagnosis is further supported by imaging studies such as the renal ultrasound and the urine albumin level. CKD is staged from levels 1 to 5. Levels 1 (eGFR 90-120 ml/min/1.73m2) and 2 (60-89 ml/min/1.73m2) CKD are significant when albuminuria or an abnormal renal ultrasound are present. Stage 3 CKD, an eGFR between 30 and 59 ml/min/1.73m2 is moderate, and is now divided into two additional stages, stage 3a and 3b. Stage 4 15-29 ml/min/1.73m2 CKD is more severe, and can often progress to Stage 5 < 15 ml/min/1.73m2, the stage where dialysis or other modalities are required.


Reference: KDIGO


Kidney disease has several causes. Most commonly it is related to hypertension and diabetes. Other diseases can lead to inflammation to various parts of the kidney’s anatomical structures. They are known as glomerulonephritis (inflammation of the glomerular filters) and interstitial nephritis (inflammation of the supporting interstitial structures). Obstruction of urine from any cause can lead to kidney disease. Some kidney diseases, such as polycystic kidneys and Alports syndrome, are inherited. Genetic disorders can result in abnormalities to the kidney structure that can set up a predisposition to develop kidney disease.


Reference: NIDDK: Causes of CKD


It is necessary to control diabetes and hypertension both to prevent and to help avoid worsening disease. Since there are so many factors in play, strict control alone may not be sufficient once the disease passes a certain point. However, strict control of these two disease helps reduce the chance of heart failure, stroke, blindness, progression of peripheral vascular disease. These disorders are commonly associated with kidney disease. Many medications that control the blood pressure will also have a protective effect on the kidney. The best known and most studied are the converting enzyme inhibitors such as listinopril and angiotensin receptor blockers such as valsartan. There are many studies that show that specific medications used to treat diabetes may also protect the kidneys. A simple way to control diabetes and hypertension is through diet, in particular through the restriction of unsaturated fats and highly refined sugars and carbohydrates with respect to diabetes, and with a salt restricted diet with regard to hypertension. Also, kidney disease can be delayed through the reduction of excess dietary protein.


When the kidneys have reached the point where they no longer can rid the body of wastes, control fluid and electrolyte balance, eliminate excess body acids or make essential hormones such as activated vitamin D and erythropoietin (required to control anemia) then renal replacement may be necessary. The term end stage renal disease (ESRD) has been used to describe this point.


There are three common therapies to help sustain well being after the kidneys fail. Each of these therapies work well and many patients rotate between them during the duration of their disease. The kidney transplant is optimal because it helps the patient return to a normal lifestyle. A donated kidney can either come from a friend or relative, or from an unfortunate accident victim who has sustained brain death. Peritoneal dialysis is ideal for many patient because it allows the patient to continue dialysis at home. It helps conserve resources because it is less labor intensive, and much of the care can be provided by the patient. Hemodialysis can also be done at home, and it takes a patient a few weeks to master the technique. It can also be done in a dialysis center for those whom home therapy is not appropriate. Surveys have demonstrated that most doctors would prefer home dialysis if given the choice. Many patients have not been introduced to home therapy or a kidney transplant early in the course of their disease, well before reaching end stage. If given an earlier opportunity, these patients would have chosen a preemptive Kidney transplant or home therapy. Often this allows the patient to remain more independent, to continue working and to travel. If you have kidney disease, be sure to ask your doctor about alternate modalities for care. There are several opportunities and resources that can help you learn more about this.


If a patient selects hemodialysis, blood must be passed through a dialysis filter. There are three major ways for this to happen. The safest and best is the arteriovenous fistula. Here a surgical procedure creates a connection between an artery and vein, generally in the lower arm, but also in the thigh in some circumstances. As this connection heals, the veins become enlarged. They support the high blood flows necessary for an adequate dialysis.


The fistula takes 6 to 12 weeks to mature. Sometimes, it takes even longer. We recommend fistulas in stage 4 CKD, generally when the eGFR reaches 20 ml/min/1.73m2. First, you should be scheduled for the vessels to be mapped, so that a suitable artery and vein can be selected. Then, a fistula placement can be scheduled by a surgeon. You will need a preoperative evaluation. Scheduling a procedure with the surgeon may take extra time. After creation, you will need to be followed up in about four weeks to make sure that it is developing as it should.


A well placed fistula lasts longer and has a lower rate of infection than a graft. Both are far better than a catheter. The catheter is a plastic tube that extends into the border of your heart. It can introduce bacteria into your blood system and cause infections. Also, it can lead to blockage known as thrombosis or a narrowing of a major vein, also referred to as stenosis. It promotes chronic inflammation that makes you sicker. Also, because the diameter of the catheter is smaller than that of the fistula or graft, less blood flow can occur, and waste products are not removed as effectively.


This depends on you, and is based on your preferences. Peritoneal dialysis is ideal for many patients because it allows them to remain independent. Some patients prefer hemodialysis, and that to can be performed in the home, to allow continued freedom with ones lifestyle. Peritoneal dialysis allows for the preservation of lifestyle, frees the arms from surgical procedures, and does not result in a difference in mortality. Many patients prefer hemodialysis in center because they do not have home support, or have a physical impairment.


Absolutely. Iit is a repetitive procedure that can easily be mastered by many people who have mastered far tougher skills at their workplace. It takes a meticulous dedication to follow a strict medical procedure, as does peritoneal dialysis. It is becoming more popular as people realize that it is not as difficult as previously thought.In many circumstances, provided you have a suitable partner, both of you learn how to operate the dialysis machine at your home. The advantages are that you can dialyze when you want to and do not need to stick to a rigid schedule. Kidney Associates doctors and assist with your training, and after you go home,  will still closely follow you and make sure your treatments are going well.


The dialysis prescription is based upon many factors. Physicians use an index known as the Kt/V as a guide to how much therapy you will require. The absolute minimum amount of therapy should give you a Kt/V greater than 1.2 if calculated by the single poor technique. If the equilibrated Kt/V measurement is used, the Kt/V should be greater than 1.4. It usually takes 4 hours to achieve this using modern dialyzers and having good blood flow. Sometimes, catheter patients require longer times. Since dialysis not only removes wastes, but also fluids, you might need to have your dialysis tailored to remove adequate fluids also.   Several studies have influenced how nephrologist write dialysis prescriptions. In one study, it was demonstrated that patients dialyzing less than 4 hours had a 42% higher incidence of death. In the other study, it was shown that as fluid removal during dialysis increased above 10 cc/kg/hour the mortality associated with dialysis increased, and was very significant at 13/cc/kg/hour. This means that for a 70 kg person running four hours – the maximum fluid removal should be less than 3640 cc. If more fluid removal, the time should be extended or the patient brought back an extra day.


References:   Assimon MM, Wenger JB, Wang L, Flythe JE. Ultrafiltration Rate and Mortality in Maintenance Hemodialysis Patients. Am J Kidney Dis. 2016 Dec;68(6):911-922. doi: 10.1053/j.ajkd.2016.06.020. Epub 2016 Aug 26. PubMed PMID: 27575009; PubMed Central PMCID: PMC5123913.


Flythe JE, Kimmel SE, Brunelli SM. Rapid fluid removal during dialysis is associated with cardiovascular morbidity and mortality. Kidney Int. 2011 Jan;79(2):250-7. doi: 10.1038/ki.2010.383. Epub 2010 Oct 6. PubMed PMID: 20927040; PubMed Central PMCID: PMC3091945.


Garg AX, Suri RS, Eggers P, Finkelstein FO, Greene T, Kimmel PL, Kliger AS, Larive B, Lindsay RM, Pierratos A, Unruh M, Chertow GM; Frequent Hemodialysis Network Trial Investigators. Patients receiving frequent hemodialysis have better health-related quality of life compared to patients receiving conventional hemodialysis. Kidney Int. 2017 Mar;91(3):746-754. doi: 10.1016/j.kint.2016.10.033. Epub 2017 Jan 13. PubMed PMID: 28094031; PubMed Central PMCID: PMC5333984.   Brunelli SM, Chertow GM,


Ankers ED, Lowrie EG, Thadhani R. Shorter dialysis times are associated with higher mortality among incident hemodialysis patients. Kidney Int. 2010 Apr;77(7):630-6. doi: 10.1038/ki.2009.523. Epub 2010 Jan 20. PubMed PMID: 20090666; PubMed Central PMCID: PMC2864594.


Eknoyan G, Beck GJ, Cheung AK, Daugirdas JT, Greene T, Kusek JW, Allon M, Bailey J, Delmez JA, Depner TA, Dwyer JT, Levey AS, Levin NW, Milford E, Ornt DB, Rocco MV, Schulman G, Schwab SJ, Teehan BP, Toto R; Hemodialysis (HEMO) Study Group. Effect of dialysis dose and membrane flux in maintenance hemodialysis. N Engl J Med. 2002 Dec 19;347(25):2010-9. PubMed PMID: 12490682.


Anemia is a condition where there are not enough red blood cells to carry oxygen to body tissues. Oxygen is necessary to generate energy in our bodies, just as it is in our car. The oxygen binds to iron and is carried by a molecule called hemoglobin inside the mature red blood cell. The kidney has a mechanism to alter the numbers of red blood cells at high or low altitudes. This is because many of our ancestors had to live in mountains at one time during our evolution. That mechanism resides in the kidney. A hormone that regulates the maturity of red blood cells, known as erythropoietin, is made by the kidney, particularly if you decide to travel to places like Colorado. In kidney disease, however, the cells that make erythropoietin are destroyed. Without erythropoietin, a patient will develop anemia. Fortunately, there are synthetic forms of erythropoietin that can replace it in patients with CKD.


Metabolic acidosis occurs when there the acids generated by the body cannot be eliminated. With respect to chronic kidney disease, our diet has acids and our kidney plays a major role in their elimination. When they accumulate they decreased cellular function, resulting to decreased appetite, an abnormal breakdown of muscle, and chronic debilitation. Recent studies show that adding bicarbonate to the diet, either with oral supplements, or with at least three cups of fruits and vegetables per day, will help preserve kidney function.

Metabolic alkalosis can occur in chronic kidney disease when there is too much alkali in the system. Dehydration and diuretics are the most common causes seen in outpatient practice. Some genetic disorders can cause alkalosis, but are rare. Chronic lung disease may be associated with a metabolic alkalosis compensating for abnormal pulmonary respiration.


Electrolytes are simply fluids that can carry an electrical charge or an electron. They are important to help transfer the tiny electrical forces that drive the chemical reactions that make your body function smoothly. There are many chemical reactions constantly taking place inside your body. Many of these involve the transfer of energy from the food that you eat and oxygen from the air you breath. The oxygen and broken down food products are carried by blood to the cells that make up your body tissues. The oxygen donates an electron that causes energy to be stored for when it will be needed. The electron then passes through a chain of chemical reactions where it combines to form carbon dioxide and water. The carbon dioxide is then exhaled.


The kidneys both eliminate phosphorus and activate vitamin D. When kidney disease occurs, factors such as FGF23 help augment phosphorus excretion, but this is bad for the heart. Other factors such as klotho are decreased in this process, and this has been shown to be beneficial. As the phosphorus levels increase, bone calcium is released as a buffer, and this process is controlled by glands in the neck known as parathyroid glands. Thus parathyroid hormone levels are increased to achieve calcium phosphorus balance. However, this hormone often creates more harm than good by reabsorbing too much calcium from bone. Unfortunately, the decreased calcium in bone and the increased phosphorus in the circulation results in a type of hardening of the arteries known as medial calcification. This puts a strain on the heart because blood vessels stiffen, increasing the resistance agains which it must pump. To minimize these problems your doctor will work with you to reduce the intake of phosphorus, particularly in processed foods. You may also require products to bind dietary phosphorus. Other medications such as vitamin D analogues and drugs specifically designed to lower parathyroid hormone may be used as your disease advances. Some patients require surgery to remove some of the excess parathyroid gland tissue that is contributing to the problem of vascular calcification.


Albumin is a protein. We are all familiar with albumin because it makes up the yolk of the eggs we eat or cook with. Our body makes albumin when we are healthy, but when we become ill, it must make molecules that are associated with inflammatory processes associated with illness. The inflammatory processes also cause a loss of appetite. A low serum albumin is a sign of chronic illness. Although we should try to maintain good nutrition when we are sick, unless we successfully fight the underlying chronic illness, the serum albumin levels will remain low.


Although, office patients will mostly be managed for chronic kidney disease, sometimes kidney disease occurs suddenly and unexpectedly. It may follow a difficult surgical procedure, the ingesting of a toxic medication, or acute trauma. Hemorrhage and tissue injury can result in acute kidney injury. It is no surprise that it was first noticed as a result of wartime trauma. When acute kidney injury is diagnosed in the critically ill patient, nephrologist play a major role in treating the disease with either acute hemodialysis or alternate forms of renal therapy known as chronic veno-veno hemodialysis.


Acute kidney injury can be prevented on an outpatient basis by careful attention to the use and combinations of medications, particularly non steroidal anti inflammatory drugs such as ibuprofen and naproxen. Dehydration and diuretics can cause acute kidney injury. (AKI). Contrast media and many other medications can result in AKI. The use of proton pump inhibitors (PPIs) such as omeprazole for prolonged periods of time can also cause kidney disease. In many circumstances AKI is mild, completely recovers, and does not lead to future problems. However, this is not always the case. The presence of AKI in the past should lead to caution when surgery is contemplated or when medications are reviewed.


Patients with chronic kidney kidney disease are very prone to develop acute kidney injury. It is particularly risky when undergoing major surgical procedures such as a coronary artery bypass or aneurysm repair. Doctors and patients should be highly aware of this risk and try to minimize AKI by judiciously reviewing medication lists, avoiding radioiodinated contrast agents unless absolutely necessary, and assuring patients are maintaining adequate hydration. Reviewing diuretic use, and adjusting the dose appropriately, will also help prevent acute kidney injury in patients with underlying CKD.

It should be noted that once a patient has CKD, the diminished kidney reserve will lead to larger spikes in the serum creatinine related to fluid balance, acute infection, or the control of blood pressure. Oftentimes these spikes are reversible. (Refer to Chapter 5, Reversing the Reversible in Essentials of Chronic Kidney Disease, Stephen Fadem, Editor, Nova Science Publishers, Hauppauge, NY, 2018)

AKI was once thought to be reversible, and that once a patient recovered from it, there would be an unlikely chance it would cause further damage. Upon further examination, it was found that patients who had sustained AKI had a higher risk to develop progressive CKD. AKI is now known to be an independent risk factor for progressive CKD. The mechanisms for this are not clear, but it may well be that the repair process after AKI leads to local damage inside the kidney that continues to cause inflammation and scarring. It may also be that the consequences of kidney injury and the restoration of the blood supply increases mediators that can cause fibrosis. (Refer to the Chapter 13, Acute Kidney Injury in Essentials of Chronic Kidney Disease by Biruh Workeneh, Edited by Stephen Fadem, Nova Science Publishers, Hauppauge, NY, 2018).


Acute kidney injury (AKI) may follow trauma such as hemorrhage from a gunshot or knife wound, blast injury from an explosion or earthquake, or a major surgical procedure where the blood pressure is abnormally low during the procedure. It can also be causes by the contrast media used in heart catheterizations or common over the counter medications like non steroidal antiinflammatory drugs (NSAIDS) like ibuprofen or protein pump inhibitors (PPIs) like omeprazole. Sometimes, antibiotics used to treat infections and chemotherapy for cancer therapy can also cause AKI.


Glomerulonephritis means inflammation of the filtering unit of the kidney, known as the glomerulus. Symptoms may appear as the consequence of proteinuria. The loss of protein in the urine, when significant, can lead to the nephrotic syndrome. Patients with significant protein in the urine should see a nephrologist who is experienced in treating glomerunlonephritis.


There are many causes, some primary, others related to underlying medical conditions. Glomerulonephritis can be of slow onset, or appear rapidly. When it occurs slowly, primary causes can be either focal sclerosis glomerulonephritis, IgA nephropathy, idiopathic membranous glomerulonephritis, minimal change glomerulonephritis or membranoproliferative glomerulonephrtitis.These disease are often diagnosed by a kidney biopsy, and are often treatable. They are often treated with medications, and their response to therapy can be variable. Sometimes, their management is a long term, chronic process.
Sometimes, the inflammation may be rapid. The body has a system to fight infections and foreign substances known as the complement system. There are three ways that the complement system can be activated, the classic pathway, the lectin pathway and the alternate pathway. C3 glomerulonephrtitis is very rare, but causes activation through the alternate pathway. This leads to an acute and rapid inflammatory response, and leads to damage to the kidneys. Early efforts at treatment are necessary to try to minimize or avoid this damage.
Sometimes the antibody response is directed against the grannules inside white blood cells – antineutrophil cytoplasmic antibodies (ANCA). This can cause disease known as Wegeners granulomatosis or polyarteritis nodosa. Goodpastures disease is a rare disorder where an acute antibody reaction occurs to the glomerular membrane and to membranes in the lung – known as anti glomerular basement (Anti GBM) antibodies. These diseases can lead to rapid deterioration in kidney function as well as other systemic effects. They are severe and require immediate attention and management. Their prognosis may not be as good as other types of kidney disease. Since these disorders affect blood vessels, they cause a condition known as vasculitis. This can be serious and requires prompt attention.


Glomerulonephritis can be secondary to underlying conditions such as systemic lupus erythematosis, sickle cell disease, diabetes, HIV, hepatitis, and a variety of other conditions. Like primary glomerulonephritis, it requires attention, and often a kidney biopsy is necessary. Treatment strategies may focus on management of the underlying disease, but the presence of kidney disease makes therapy more important since it is the kidney disease progression to end stage that often leads to the major complication of many other disorders.


Sometimes kidney inflammation occurs within the supporting structures of the kidney. When this happens inflammatory cells and edema can interfere and block the nephron tubing and cells that perform essential exchange functions as well as transport fluids. Certain medical conditions such as autoimmune disorders and infections, as well medications are the most common causes. Over the counter medications (non steroidal antiinflammatory drugs – (NSAIDS – ibuprofen, naproxen, indomethacin and several others) can cause this condition. Antibiotics are also associated with interstitial nephritis. Most often, interstitial nephritis is reversible, but can leave scarring and contribute to kidney damage and progressive CKD.
A good medical review for doctors: Raghavan R, Eknoyan G. Acute interstitial nephritis – a reappraisal and update. Clin Nephrol. 2014 Sep;82(3):149-62. Review. PubMed PMID: 25079860; PubMed Central PMCID: PMC4928030.


Chronic kidney disease reduces the amount of kidney function that you have, and thus diminishes kidney reserve. Medications that can harm the kidney concentrate to only the functioning part of the kidney, and can damage it further. NSAIDS have been shown to damage the kidney, decreasing the amount of blood flowing to the deeper parts of the kidney, and by setting up an inflammatory response. This may be reversible in people with perfectly normal kidney function, but in persons with preexisting kidney disease, may not be completely reversed, and can contribute to disease progression.
Prolonged use of NSAIDS is associated with progressive kidney disease.
Reference: Gooch K, Culleton BF, Manns BJ, Zhang J, Alfonso H, Tonelli M, Frank C,
Klarenbach S, Hemmelgarn BR. NSAID use and progression of chronic kidney disease.
Am J Med. 2007 Mar;120(3):280.e1-7. PubMed PMID: 17349452.


The MRI itself is not particularly dangerous, unless you have metal implants. However, the contrast agent used in an MRI, gadolinium, can cause serious consequences and can lead to systemic scarring. Thus, it is prudent to avoid gadolinium-based contrast agents in patients who have CKD.
Reference: Agarwal R, Brunelli SM, Williams K, Mitchell MD, Feldman HI, Umscheid CA.
Gadolinium-based contrast agents and nephrogenic systemic fibrosis: a systematic
review and meta-analysis. Nephrol Dial Transplant. 2009 Mar;24(3):856-63. doi:
10.1093/ndt/gfn593. Epub 2008 Oct 24. Review. PubMed PMID: 18952698.


Kidney transplants can either be planned or unplanned. Planned transplants are either from a living relative, a friend, or from a paired donor arrangement. In each case a donor, found to be in excellent health, volunteers to donate a kidney that is implanted into a waiting recipient. Surgeries are concurrent. Although living related donors have the best chance of survival because inheritance reduces the immune reaction, the use of medications developed and tested over the last 40 years, has markedly increased survivalists of kidneys from non-related donors. In the paired donor program, donor A and recipient A may not have the same blood type, and are incompatible. But, another donor, donor B is compatible with recipient A, while recipient B is compatible with donor A. The four surgeries are done concurrently, and each recipient receives a compatible match.


The risk is small, but there is a risk that one will develop kidney disease more rapidly with one kidney, rather than with two, particularly if one remains healthy with respect to risk factors such as salt intake, blood pressure control, smoking cigarettes, and remaining active. There is always the chance that there can be a complication of donor surgery, and that the donor may have trauma that could injure remaining kidney. Again, these risks are small. The living donor should become well informed of risks and benefits of this procedure before making any decision.


Gout is a type of arthritis that is caused by the deposition of uric acid crystals. It is strongly associated with kidney disease, mainly because as CKD progresses, uric acid excretion by the kidneys decreases. Gouty symptoms are common in CKD, and the American College of Rheumatology recommends treating CKD patients with uric acid lowering agents if symptoms of gout occur. The question remains whether gout can actually cause CKD to worsen. It has been observed that many patients with gout and CKD have uric acid crystal deposition in the kidney, but the extent of disease is greater than these findings. Uric acid metabolism is also related to the metabolism of sugar, the presence of oxidation-causing reactions that harm blood vessels, and the presence of diabetes. Thus far, we have much to learn about the association between gout and CKD, and whether specific treatment of CKD patients with uric acid lowering agents will help protect against its progression.  Reference:Johnson RJ, Nakagawa T, Jalal D, Sánchez-Lozada LG, Kang DH, Ritz E. Uric acid and chronic kidney disease: which is chasing which? Nephrol Dial Transplant. 2013 Sep;28(9):2221-8. doi: 10.1093/ndt/gft029. Epub 2013 Mar 29. Review. PubMed PMID: 23543594; PubMed Central PMCID: PMC4318947.


HIV is a virus that interacts with the immune system and destroys the white cells known as T-helper cells or CD4 cells. Since it harms the system, it perpetuates itself, and also making the victim susceptible to infections. This is termed immunodeficiency, and the disease it causes is known as the acquired immunodeficiency disease or AIDS. The diseases caused by AIDs can be fatal, but luckily there is treatment.   HIV is present in the blood and body secretions of infected persons, and thus spread by sexual contact, or the use of needles that have not been sanitized. The disease has a latency period, and thus one cannot be sure a contact is infected. Since dialysis units deal with blood on a constant bases, and since there is uncertainty as to who among the patients is infected, the CDC has recommended universal precautions – treating every patient, utensil and device as potentially contaminated. This is why, upon entering a dialysis center, one is always required to wear personal protective equipment (PPE, such as gowns), and wear gloves and sanitize hands when in contact with a patient or dialysis machine.   The body tries to defend against HIV, and one of the defenses, is the increased release of interferon. In fact, some subtypes of interferon increase products that may help fight viral attacks, and may be effective against HIV. One factor increased by interferon is APOL1. Some person, particularly those of Western African descent, have a high likelihood of having two copies of a variant of APOL1, and that variant is also increased. APOL1 variants are associated with the development of advanced CKD. In these patients with have two variant APOL1 copies, there is a high incidence of kidney failure. Thus HIV is associated with a type of glomerulonephritis that advanced kidney disease progression, particularly in African Americans with two copies of variant APOL1.


There are mainly four types of kidney stones, calcium oxalate, uric acid, calcium pyrophosphate and cystine. Passing a kidney stone is very painful. This is generally severe, comes and goes, starts in the flank and radiates to the front. It is known as renal colic. Renal colic occurs when the stone is in the ureter, pressing against the sensitive ureter walls. Often times, urologists can remove the stones before they pass, and in many instances, the nephrologist can analyze the kidney stone and help prevent its recurrence or even dissolve it using medications and dietary adaptation.   Whether to manage a kidney stone medically or using an intervention has been discussed by the American Urological Association. The AUA reviewed 1,911 articles when issuing their 2016 guideline statements ( Medical management is prudent for smaller stones, those less than 8-10 mm, as many can pass spontaneously, or with the use of medical expulsive therapy. The meta-analysis that was done by the American and European urological associations identified that when stones were ≤ 5 mm, 68% pass spontaneously. When stones are > 5 mm and ≤ 10 mm, 47% pass spontaneously.


Reference: Preminger GM, Tiselius HG, Assimos DG, Alken P, Buck C, Gallucci M, Knoll T,
Lingeman JE, Nakada SY, Pearle MS, Sarica K, Türk C, Wolf JS Jr; EAU/AUA
Nephrolithiasis Guideline Panel. 2007 guideline for the management of ureteral
calculi. J Urol. 2007 Dec;178(6):2418-34. Review. PubMed PMID: 17993340.


Active surveillance is appropriate for patients who are asymptomatic, but clinicians may offer stone treatment for patients who are symptomatic with flank pain. 95% of stones > 8 mm require intervention by a urologist.

Terminology associated with kidney stones:
SWL – shockwave lithotripsy
URS – ureteroscopic lithotripsy
PCNL – percutaneous nephrolithotomy
MET – medical expulsive therapy


Calcium oxalate stones – These are most common and occur when one drinks inadequate fluids, eats excess protein or salt, or a diet high in foods containing excessive oxalate. Persons with colitis may also have increased oxalate absorption. Stones occur when their is too little fluid in the kidney environment to keep salts from forming crystals. Excess oxalate containing foods include nuts, beets, soy, bran, and Swiss chard. Persons should not avoid oxalate containing foods altogether. It is not necessary. Vitamin C can also potential oxalate stones. These can be prevented by adequate hydration, the use of potassium citrate (that helps dissolve stones) and sometimes thiazides diuretics (that potential calcium reabsorption.


Uric acid stones – These stones may not appear on a plain film, but will be detectable on a renal ultrasound. They can occur when the uric acid is high and in the presence of an acidic urine. Persons with gout may have a higher incidence of uric acid stone. They can be dissolved in many cases. Using conventional medical therapy- alkalization of the urine, encouraged hydration and an xanthine oxidase inhibitor such as allopurinol, it may take several months for a uric acid stone to dissolve.


Struvite stones – This is less common than uric acid or calcium oxalate as the cause of kidney stones. Struvite refers to a mineral made by bacteria, and these hard, large stones are caused by bacterial infections. They may encompass the entire renal pelvis, forming what is referred to as staghorn calculi. They are associated with an alkaline urine, hence acidification of the urine is optimal. These stones may require more than medical management.


Cystinuria – This is extremely rare because it is an autosomal recessive disorder. It is a genetic diorder where cysteine can accumulate in the kidney and form stones. The child must inherit a copy of the gene from both parents to develop the disease. There is no treatment for cystinuria.


The most common inherited kidney diseases are autosomal dominant polycystic kidney disease (ADPKD) and Alport syndrome. Fabry disease is rare. There are a host of urological disease that are inherited, and occur in childhood. Some patients inherit tubular defects that cause syndromes that interfere with acid-base and electrolyte metabolism. The most common of these diorders are Barrter Syndrome, Gittelman Syndrome and Liddle Syndrome.


Autosomal dominant polycystic kidney disease is an inherited disorder where a gene defect causes the kidney to create cysts. As these cysts grow, they block normal kidney tissue, and result in kidney damage. In PCKD the kidneys are enlarged. Early signs may be the inability to form a concentrated urine. Recently, a new therapy for PCKD was approved by the FDA.


Alport Disease is a sex-linked genetic disorder that is characterized by a defect in collagen formation. Thus, the basement membrane of the glomerular filter, an area that contains collagen is weaker, and over time, wear and tear on the membrane results in permanent kidney damage. Patients with Alport Disease also have impaired hearing and an eye condition.


Another sex linked disorder Fabry disease. Here there is a defect in galactosidase, leading to an accumulation of galactoside in the cells of the heart and kidney. There are several signs and symptoms that characterize this disorder. Patients may have heart failure as well as kidney disease. They may also have an impaired ability to perspire, and small, dot-like red lesions on their hands and torso. There is now a treatment that can help prevent its progression.


In Western Africa, there exists a parasite known as the trypanosome. It is spread by a fly that bites and draws blood – the tsetse fly. This disease is defined by the encephalopathy it produces, the African Sleeping Sickness, and by its medical disease – trypanosomiasis. The body creases a defense against the trypanosome by increasing APOL1. APOL1 is able to enter an important organelle in the parasite known as the lysosome, and destroy it. However, through the years of evolution, the parasite developed a defense against APOL1, and APOL1 variants evolved to fool the trypanosome parasite. Thus, many Africans became immune to trypanosomiasis, and since the APOL1 variant was inherited, this immunity was passed from one generation to another. However, persons whose mothers and fathers both had an APOL1 variant, that is, those who had a copy of the gene from each parent, were more likely to have sclerosis of the kidneys and to develop kidney failure. For this reason, the incidence of kidney disease is nearly 5 fold higher in persons of Western African descent.


Since APOL1 is related to the defense against disease, certain infections can stimulate its presence through defense mechanisms such as interferon. Thus, if a variant in APOL1 is present, the incidence of certain conditions such as HIV1, and systemic lupus, can also increase the incidence of advanced CKD.