Clean kidneys promote improved functions and prevent impairment so attain the benefits with these proven measures of Ayurvedic treatment for cleaning kidneys.

Foods for kidney cleansing is an exclusive meal plan, developed by experts, to help you cleanse your kidneys. Learn more here.

Your kidneys are remarkable organs situated on either side of your spine, below the ribs. They play vital roles in maintaining your overall health by

For your health, the kidneys are essential because they detoxify and cleanse the body by filtering 10–150 quarts of blood in a day….

Overview of the digestive system—how food moves through each part of the GI tract to help break down food for energy, growth, and cell repair.

For urologists and their patients, this 20" x 26" (51 x 66 cm) exam-room anatomy poster with grommets illus­trates the following diseases for both males and females: chronic pyelo­nephri­tis, multiple renal calculi, glomerulo­nephritis, acute renal failure, stag­horn calculus, papil­lary necrosis, reno­vascular hyper­tension, renal artery stenosis, adeno­carci­noma of kidney, transi­tional-cell carci­noma of renal pelvis bones and more. Published by Wolters Kluwer. ©2000< Order at least 2 please Laminated with 2+ corner grommets Illustrates nearly 30 genitourinary disorders

Learn how treatments and lifestyle changes might help reduce damage to your kidneys from polycystic kidney disease.

OVERVIEW OF CHRONIC KIDNEY DISEASE Chronic kidney disease (CKD) affects over 26 million adults in the United States and is defined as 3 or more months of either (1) histopathologic or functional evidence of kidney damage, or (2) a glomerular filtration rate less than 60 mL/min/1.73 m2. CKD is classified into five stages based on the degree of functional impairment, as inferred from estimations of glomerular filtration rate. CKD can be caused by numerous underlying processes. In general, causes can be grouped into glomerular diseases (such as diabetic nephropathy or lupus nephritis), vascular diseases (such as hypertension), tubulointerstitial diseases (such as obstructive uropathy), and cystic diseases. The most common causes are diabetes mellitus and hypertension, which together account for over two thirds of cases. PATHOPHYSIOLOGY Irrespective of the primary renal disease, the kidney initiates a compensatory response to nephron loss that is initially adaptive but ultimately causes further loss of function. Thus the progression of CKD depends in part on mechanisms that are independent of the inciting disease process. In particular, loss of a subset of nephrons results in compensatory hyperfiltration and hypertrophy of the remaining functional nephrons, an effect likely mediated by angiotensin II, aldosterone, endothelin, and other hormones. The resulting intraglomerular hypertension, however, eventually becomes maladaptive, inflicting damage to the remaining nephrons and thereby causing a further decline in overall filtration. In the glomerulus, podocyte (visceral epithelial cell) foot process effacement and denudation may lead to a breakdown of the protein filtration barrier and glomerulosclerosis. The ensuing proteinuria is thought to further promote kidney failure by exerting toxic effects on the tubules. In addition, mesangial cells respond to the increased pressure with proliferation and production of increased extracellular matrix; these changes stimulate inflammation and cellular infiltration of the mesangium and tubulointerstitium, leading to tubulointerstitial fibrosis. A significant number of nephrons must be lost before these maladaptive changes are seen, and the exact quantity varies between species and individuals. In rats, for example, one and 5/6 nephrectomy must be performed to create a model of progressive renal insufficiency. In humans, it is well-known that donation of one entire kidney does not generally result in loss of overall renal function. In those individuals who do lose enough functional renal mass to experience the maladaptive effects of hyperfiltration, the rate of further functional decline is also variable, depending on the primary inciting factor, patient age, and possibly genetic factors. ASSESSMENT OF RENAL FUNCTION The serum creatinine concentration should be used to estimate the creatinine clearance or GFR (eGFR), which can be accomplished using the Cockcroft-Gault formula or the modification of diet in renal disease (MDRD) study equation, respectively. Current guidelines recommend that serum creatinine concentration be measured at least once per year in patients with CKD. The frequency should be increased in those with an eGFR <60 mL/min/1.73 m2, loss of >4 mL/min/1.73 m2 per year of eGFR, or with risk factors for progression (high level of proteinuria, hypertension, diabetes mellitus). Patients should be referred to a nephrologist when the eGFR falls below 30 mL/min/1.73 m2, or sooner if the primary care physician is unable to carry out a treatment plan for CKD. COMPLICATIONS AND MANAGEMENT Patients with CKD are typically asymptomatic until the disease process becomes advanced. Thus it is important to screen for CKD and its complications in high-risk patients, such as those with diabetes mellitus and/or hypertension, so that treatment can be initiated at an early stage. Hypertension. Hypertension is both a cause and consequence of progressive chronic kidney disease. It is a cause because elevated arterial pressures are transmitted to the glomeruli of the remaining nephrons, exacerbating hyperfiltration and accelerating further nephron loss. It is also a consequence because, as nephron loss progresses, there is ongoing secretion of angiotensin II and impaired excretion of excess sodium and water. Thus more than 75% of patients with CKD suffer from hypertension. Blood pressure must be routinely measured in all patients, and hypertension must be treated to slow nephron loss. Blood pressure should be kept at 130/80 mm Hg or less, and the mainstays of treatment are medications that block the renin-angiotensin-aldo-sterone system, including ACE inhibitors and ARBs. These agents preferentially dilate efferent arterioles, lowering intraglomerular pressure. Because of this partial reversal of glomerular hyperfiltration, there is an expected and acceptable 30% increase in serum creatinine; however, providers should carefully monitor patients for both acute declines in eGFR and hyperkalemia. Diuretics are often needed as well, especially as more advanced disease leads to greater retention of sodium and water. In general, at an eGFR <30 mL/min/1.73 m2, loop diuretics are more effective than thiazide diuretics. Patients should also be strongly encouraged to maintain a low-salt diet. Proteinuria. Proteinuria is a marker of glomerular injury, but it is also understood to contribute to CKD progression. In particular, proteins that are filtered in the glomerulus are reabsorbed in proximal tubule cells, where they trigger inflammation, apoptosis, and fibrosis. In addition, abnormal filtration of growth factors and cytokines also promotes tubular injury. Thus a reduction in proteinuria has been associated with a slower progression of chronic kidney disease, particularly among patients with diabetic disease. Proteinuria must be regularly assessed in all patients. In nondiabetics, screening with urine dipstick is acceptable, but if positive, a spot urine protein : creatinine ratio should be performed for quantification. A 24-hour urine collection for protein can be performed; however, a spot sample is typically adequate and is easier for the patient. In diabetics, regular screening for microalbuminuria should be performed early in the disease course. ACE inhibitors and ARBs have been shown to reduce proteinuria, likely because of the reduction in intraglomerular pressure. Studies in diabetic patients have shown that these drugs reduce proteinuria and slow the decline of eGFR independent of their effect on systemic blood pressure. Bone Disease. Renal disease also leads to numerous morphologic changes in bone, a group of phenomena collectively known as renal osteodystrophy. This disorder encompasses a spectrum of disease with both high bone turnover (osteitis fibrosa cystica) and low bone turnover (adynamic bone disease and osteomalacia). Osteitis fibrosa cystica, a high turnover disease, reflects secondary hyperparathyroidism and is associated with bone pain and an increased risk of fracture. High PTH levels are often seen once the eGFR declines to less than 60 mL/min/1.73 m2 (stage 3 CKD), and they are invariably seen when eGFR is less than 30 mL/ min/1.73 m2 (stage 4 CKD). High PTH levels initially occur because of decreased renal production of 1,25(OH)2D, the activated form of vitamin D, which results from both a reduction in renal mass and impaired renal excretion of phosphate. The decline in 1,25(OH)2D stimulates PTH secretion and, moreover, causes a reduction in intestinal reabsorption of calcium, which further stimulates PTH release. Initially, the high levels of PTH maintain serum phosphate and calcium concentrations within normal range, at the expense of causing bone disease. As renal dysfunction progresses, however, hyperphosphatemia ensues. In addition, hypocalcemia eventually occurs, both because of the decline in 1,25(OH)2D levels and because of formation of soluble calcium phosphate complexes. Skeletal resistance to PTH, which remains chronically elevated, also appears to play a role. In patients with stage 3-5 CKD, serum concentrations of PTH, phosphate, and calcium should be checked regularly. According to current guidelines, the goal PTH levels for stage 3 CKD are 35 to 70 pmol/L, for stage 4 CKD are 70 to 110 pmol/L, and for stage 5 CKD are 150 to 300 pmol/L. Goal serum phosphate levels for stages 3 and 4 CKD are 2.7 to 4.6 mg/dL, and for stage 5 CKD are 3.5 to 5.5 mg/dL. To achieve these levels, hyperphosphatemia is typically addressed first using a low phosphorous diet and phosphate binders. Either calcium or noncalcium containing binders may be used, with the choice sometimes depending on the patient’s serum calcium concentration. Vitamin D (25-OH) levels should also be checked, and if levels are below 30 µg/mL, supplemental ergocalciferol may be offered. If PTH levels remain elevated despite these measures, active vitamin D analogues (such as calcitriol) may be used in lieu of ergocalciferol; however, these agents may cause marked elevation of serum phosphate and calcium levels, which must continue to be carefully monitored. In patients with more advanced disease, calcimimetics (i.e., cinacalcet) may be used, although they are only approved for those receiving dialysis. Calcimimetics bind to the calcium sensing receptor on the parathyroid glands, suppressing PTH release, but they are associated with an increased risk of hypocalcemia. If PTH levels are oversuppressed, patients can develop adynamic bone disease, which is also associated with increased risk of fracture. This disorder is becoming increasingly common as vitamin D analogues are more widely used to suppress PTH. If the PTH level falls below 100 pmol/L, the risk of adynamic bone disease is high, and dosages of vitamin D analogues and calcium-based phosphate binders should be reduced. Finally, osteomalacia, another form of low bone turn-over disease, can be seen in some patients due to vitamin D deficiency or aluminum toxicity. With the near elimination of aluminum-based binders in clinical practice, however, aluminum toxicity is now uncommon. The specific type of bone disease can be definitively diagnosed with bone biopsy, which is not routinely performed in clinical practice. Instead, the presence of bone disease is typically inferred from abnormal PTH levels. Acidosis. Once GFR declines to 40 to 50 mL/ min/1.73 m2, patients are not able to excrete their daily acid load. The remaining functioning nephrons have maximized their ammonium excretion, and excretion of titratable acids may also be reduced because of the dietary restriction of phosphate and use of phosphate binders. The result is metabolic acidosis with a positive anion gap, which is usually discovered as a low serum bicarbonate level on a routine assessment of serum chemistries. Current guidelines recommend that serum bicarbonate be checked annually in patients with stage 3 CKD and every 3 months in patients with stage 4 or 5 CKD. It is recommended that serum bicarbonate concentrations be maintained at 22 mEq/L or greater. Oral bicarbonate replacement can be used to achieve this goal. Anemia. CKD leads to normocytic anemia due to inadequate renal production of erythropoietin. Anemia is sometimes seen in stage 3 CKD and is almost always seen in stage 4 CKD. Current guidelines recommend that hemoglobin levels be measured annually in any patient with CKD. In males with hemoglobin less than 13 g/dL and females with hemoglobin less than 12 g/dL, further workup should be performed, including a complete blood count, reticulocyte count, and an assessment of iron stores. Relative iron deficiency is common and contributes to the decreased production of red cells. One reason for iron deficiency is that the inflammatory cytokines released in CKD promote secretion of hepcidin, which blocks iron absorption from the GI tract and iron release from macrophages. In general, erythropoiesis-stimulating agents are used to maintain a hemoglobin level of 11 to 12 g/dL. The target should not exceed 13 g/dL. In patients receiving this treatment, iron stores should be assessed and replenished as needed to avoid apparent erythropoietin resistance. Oral iron supplements, such as iron sulfate or iron gluconate, are commonly given. If patients are resistant to these supplements because of impaired intestinal absorption, intravenous iron preparations may be used instead. Cardiovascular Disease. Cardiovascular disease is the leading cause of death among patients with chronic kidney disease, and it affects 40% of dialysis patients compared with 10% of the general population. Patients with CKD are more likely to have classic risk factors for cardiovascular disease, such as hypertension, diabetes mellitus, and hyperlipidemia. CKD itself, however, also appears to be an independent risk factor for CVD, and recent studies have shown a strong correlation between declines in eGFR and increased cardiovascular events. Numerous factors are responsible for this association. Vascular calcification appears to result from the use of calcium-based phosphate binders and vitamin D analogues. It may affect the intimal layer, leading to atherosclerotic plaques, and/or the medial layer, leading to vessel stiffening. The inflammation and secondary hypertension associated with CKD also accelerate vascular disease. In addition to increasing the risk for cardiovascular disease, CKD also increases the risk of left ventricular hypertrophy by causing hypertension, anemia, and hypervolemia. The prevalence of left ventricular hypertrophy is much higher among dialysis patients than the general population. Modification of cardiovascular risk factors such as smoking, hyperlipidemia, and hypertension should remain a primary focus of therapy. Even after kidney disease becomes more advanced, many patients die from cardiovascular disease before ever reaching end stage renal disease. Hyperkalemia. Renal excretion of potassium does not become significantly impaired until stage 4 CKD; however, a potassium rich diet or use of ACE inhibitors/ARBs can lead to hyperkalemia at earlier stages. A low potassium diet (<50 mEq/day) may be instituted as a preventive measure. In addition, treating metabolic acidosis will lower serum potassium levels, and loop diuretics may be used to promote urinary excretion of potassium. Dialysis may be required if hyperkalemia becomes refractory to medical management. Volume Overload. Overt symptoms of volume overload, such as peripheral and pulmonary edema, do not typically occur until stage 5 CKD but can be precipitated in earlier stages by increased salt intake or coexisting congestive heart failure. These symptoms can generally be treated with sodium restriction and additional diuretics. Uremia. As renal dysfunction becomes very advanced, the retention of toxic substances in the general circulation can lead to numerous abnormalities that are together known as uremia. In general, the term is used to describe the effects of those retained toxins that have not been identified or are poorly understood. Signs and symptoms of uremia include loss of appetite, weight loss, fatigue, altered mental status, peripheral neuropathies, nausea, vomiting, pruritus, and platelet dysfunction. Although uremia is associated with an elevated blood urea nitrogen (BUN) concentration, BUN itself is not felt to be the cause of uremia. ADDITIONAL CONSIDERATIONS It is essential that renally cleared medications be dosed based on eGFR. Furthermore, drugs that may precipitate an acute decline in renal function, such as nonsteroidal antiinflammatory drugs should be avoided. Careful consideration must be given when administering iodinated contrast due to the risk of acute renal failure. In addition, gadolinium-based contrast should be used judiciously in patients with stage 4 or 5 CKD because of the increased risk of nephrogenic systemic fibrosis. END STAGE RENAL DISEASE Ultimately, a small proportion of patients with CKD will progress to end-stage renal disease (ESRD), defined as the need for dialysis therapy or kidney transplantation. The rate of progression, however, is highly variable across patients. Dialysis is typically initiated when the eGFR falls below 10 mL/min/1.73 m2; however, there are numerous acute indications as well, which include refractory hyperkalemia, volume overload, and uremia. In most patients, preemptive kidney transplantation is preferred over ongoing dialysis because the long-term survival is significantly better. Compared with dialysis patients on the transplant list, patients who receive a kidney transplant have an initial increase in mortality; however, at 4 months post-transplant the risk of death is equal between the two groups, and thereafter transplanted patients have a 68% lower risk of mortality compared with patients on dialysis. The survival benefit is particularly robust among patients with diabetes.

If you are looking for a solution for solving your renal issues, then keep reading... Going through life with major organ failure is a tough endeavor. You can neither do the same things nor eat the same food you used to, and if you decide to slack off from caution, it could result in an adverse outcome. Everything should be checked and done with care. To maintain a steady monitored life, you need all the information you can get from what foods to eat, what to avoid, and why certain foods need to be avoided. In a state of compromised health, the last thing you need to do is to worry aimlessly about every single aspect. Details of certain kidney diseases are provided. All the aspects you need to know about renal dieting are provided later on, from foods to eat to how to live a much more fulfilling and stress-free life following them. Here, details of making easy to-go meals and meal planning are discussed. Also, nutritional information is given and tips on how to customize them according to your taste. If you have been recently diagnosed with chronic kidney disease or have any illness regarding the renal system, then you first need to understand that there are thousands of people in the world living good lives with diseases such as yourself. It is not the end of the world, and with proper care and lifestyle changes, you can start living a happy life as well. Whether recently diagnosed or not, this dieting plan will reduce the load on your kidneys and help you live a healthier life. To care for yourself is to care for your loved ones too. Your life is important to everyone that is precious to you, and you must improve as much as possible. This book covers the following topics: - What's the kidney? What's it for?- Introduction to power supply- Diet plan- Recipes...And much moreKidney problems are complicated and require adequate management. Diet is an integral component of treatment for kidney disease and the best way to prevent potential complications such as dialysis or organ transplant. A renal diet is easier to follow than most people think once you understand what to eat and avoid. The main purpose of this book is to introduce you to the world of renal diet and show some delicious yet healthy foods you can prepare easily in your kitchen. Throughout the pages of this book, you'll learn more about kidney diseases and their causes, but also get valuable insight into renal diet, find out what you should eat and avoid, and so much more. Of course, the central component of the book is a cookbook with a 14-day renal diet plan, 60 recipes, and easy instructions. The best thing about this cook is simplicity. All recipes are easy to make and feature accessible ingredients that won't be difficult to find, buy, and use. With our cookbook, you'll be able to improve the function of your kidneys and cut this risk of dialysis. This is also a great present for someone who has kidney disease and struggles to manage it. So, let's get started!

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POLYCYSTIC KIDNEY DISEASE Polycystic kidney disease is an inherited disorder that exists in both autosomal dominant and autosomal recessive forms (ADPKD and ARPKD, respectively). Both diseases are characterized by the bilateral, diffuse formation of renal cysts that replace normal parenchyma and cause progressive renal insufficiency. ADPKD ADPKD is a relatively common condition, with a prevalence of 1 : 400-1 : 1000, and it is responsible for approximately 5% to 10% of end-stage renal disease (ESRD). Most cases reflect autosomal dominant inheritance of the mutated gene from an affected parent, with complete penetrance; however, about 5% of patients have parents with normal kidneys, suggesting a de novo genetic mutation. ADPKD is caused by mutations in the genes PKD1 (chromosome 16p13.3) or PKD2 (chromosome 4q21). PKD1 mutations account for 85% of cases, whereas PKD2 mutations account for the remainder. PKD1 encodes polycystin-1, an integral membrane protein thought to play a role in cell-cell and cell-matrix interactions, while PKD2 encodes polycystin-2, a cation channel involved in calcium signaling. Although polycystin-1 and polycystin-2 appear to interact with each other at primary cilia, the precise mechanism by which mutations in these proteins cause cyst formation remains unclear. It is generally accepted, however, that cystogenesis follows a two hit model. Although most renal tubules possess epithelial cells that contain one mutated allele and one normal allele, a small subset possess cells in which the normal allele also becomes mutated, which is the second “hit” that permits cyst formation. There is a wide range of clinical phenotypes associated with ADPKD, ranging from a complete lack of symptoms to progression to ESRD. When symptomatic, the disease usually first presents in the third to fifth decade as flank pain and hematuria (reflecting either traumatic or atraumatic cyst rupture, nephrolithiasis, or infection), hypertension, and progressive renal insufficiency. Extrarenal disease manifestations are common, and they include hepatic cysts (in approximately 80%), pancreatic cysts (in approximately 10%), intracranial aneurysms (in approximately 10%), and mitral valve prolapse (in approximately 20%). To some extent, the rate at which renal insufficiency progresses is dependent on the specific underlying mutation. Patients with PKD1 mutations, for example, develop ESRD at a mean age of 54 years, whereas those with PKD2 mutations develop ESRD at a mean age of 74 years. Even within the subgroup of patients with PKD1 abnormalities, those with mutations near the 5’ end of the gene generally have a slightly faster progression to ESRD than those with mutations located near the 3’ end (53 years versus 56 years, respectively). ADPKD can be diagnosed using several imaging modalities-such as ultrasound, CT, or magnetic resonance imaging-which reveal enlarged kidneys that possess diffuse, fluid-filled cysts. The cysts are variable in size, ranging from several millimeters to several centimeters, and are present in both cortex and medulla. The differential diagnosis should include other entities such as simple cysts (see Plate 2-14), especially when few cysts are seen; renal cyst formation secondary to other genetic syndromes, such as von Hippel-Lindau syndrome or tuberous sclerosis; medullary cystic kidney disease complex (see Plate 2-18); acquired cystic disease; and ARPKD, especially if cysts are noted early in life. The specific diagnosis of ADPKD can generally be reached based on the radiographic appearance of the kidneys, the presence of associated abnormalities (e.g., hepatic cysts), and a family history consistent with auto-somal dominant transmission. Recent work has proposed the following sonographic criteria for the diagnosis of ADPKD in at-risk patients with families of unknown genotype: at least three unilateral or bilateral cysts in those 15 to 39 years of age; at least two cysts in each kidney in those 40 to 59 years of age; and four or more cysts in each kidney in those greater than 60 years of age. Due to the size and complexity of the PKD1 and PKD2 genes, genetic testing is not commonly performed. At present, no directed treatment is available to prevent or slow further cyst formation, although several experimental therapies are being studied. Instead, treatment is chiefly directed at reducing the morbidity associated with complications of the renal cysts, such as pain, hemorrhage, infection, and hypertension. If pain becomes severe, some centers offer laparoscopic unroofing of cysts or percutaneous aspiration of cyst fluid and injection of sclerosing material. Hepatic cysts are usually asymptomatic, but in rare cases portal hypertension may occur. About 10% of those with ADPKD and intracranial aneurysms will die of subarachnoid hemorrhage; however, screening for intra-cranial aneurysms is generally not performed unless there is a family history of aneurysm rupture, the patient has a high-risk occupation (e.g., pilot), or there are concerning neurologic symptoms. If progression to ESRD occurs, dialysis or renal transplantation is required. Before transplantation, nephrectomy may be necessary not only to relieve symptoms associated with the enlarged kidneys, but also to provide space for the graft. ARPKD ARPKD is a much rarer condition than ADPKD, occurring in approximately 1 : 20,000 live births. It is caused by mutations in the gene PKHD1 (located on chromosome 6p21), which encodes a protein known as fibrocystin. Fibrocystin is localized to the primary cilia of epithelial cells in the thick ascending limb and collecting duct, as well as to epithelial cells lining the hepatic biliary ducts. Although fibrocystin appears to interact with polycystin-2, it is uncertain how abnormalities in this system result in cyst formation. As with ADPKD, there is a wide range of clinical phenotypes, but patients present much earlier in life. All patients with ARPKD have congenital hepatic fibrosis, and some patients also have dilation of the intraductal biliary ducts (Caroli disease). In general, there is an inverse correlation between the severity of the renal disease, which typically presents during the neonatal period, and hepatic disease, which typically presents during late childhood or adolescence. In patients with severe renal disease, the diagnosis is first apparent using prenatal ultrasound. The kidneys appear enlarged and hyperechogenic owing to the presence of innumerable cysts. Unlike in ADPKD and most other cystic diseases, however, the individual cysts are generally too small to be visualized. If renal dysfunction is severe enough, oligohydramnios may also be present. During delivery, the enlarged kidneys may cause dystocia. Shortly after birth, the neonate may experience respiratory distress if pulmonary hypoplasia has occurred secondary to oligohydramnios or if the kidneys are large enough to cause restrictive lung disease. Patients with milder renal disease may not present until childhood, when renal insufficiency manifests as electrolyte disturbances or hypertension. Unlike in ADPKD, hematuria and infection are not common features. Patients with the mildest renal disease often present in late childhood or adolescence with symptoms referable to hepatic disease. In these patients, progressive hepatic fibrosis can result in portal hypertension, which can manifest as bleeding varices or splenic enlargement with cellular sequestration. Intrahepatic biliary duct dilation, if present, may also present as cholangitis. The diagnosis of ARPKD is generally established based on the sonographic appearance of the kidneys, described previously, in association with evidence of hepatic fibrosis and a family history that demonstrates autosomal recessive transmission. If the diagnosis is in doubt, or if family members wish to establish their carrier status, genetic testing is available. Renal biopsy is seldom performed, but the major feature is the presence of elongated cortical and medullary cysts that arise predominantly from collecting ducts. As with ADPKD, no directed treatment is available to prevent or slow cyst formation, and thus care should be directed toward managing complications of renal or hepatic dysfunction. Patients who present early in life with renal dysfunction require aggressive support to maintain adequate nutritional status and avoid sus-tained fluid or electrolyte abnormalities. Patients who have portal hypertension complications may require intervention, such as portosystemic shunting or variceal sclerotherapy. The timing of ESRD onset is variable, but when it occurs dialysis and renal transplantation become the only remaining therapeutic options.

Do you need a low potassium menu for when levels are high? Read on for some great options to add to your diet.

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Located on either side of your body, your kidneys work 24x7 to ensure that you can stay in the prime of your health all the time. But if you’re not careful

Uric acid is produced when the body breaks down fructose and nucleotide molecules (specifically, the purine bases that are part of DNA's structure). Normally, the kidneys process and excrete uric acid. Hyperuricemia occurs when uric acid crystals are not excreted properly, causing them to build up

Magnesium is an important mineral for everyone, but it's particularly important for people with AFib. Learn more about magnesium for atrial fibrillation.

Foods for kidney cleansing is an exclusive meal plan, developed by experts, to help you cleanse your kidneys. Learn more here.

What is Minimal Change Disease? Minimal Change Disease (MCD for short) is a kidney disease in which large amounts of protein is lost in the urine. It is one of the most common causes of the Nephrotic Syndrome (see below) worldwide. The kidneys normally work to clean the blood of the natural waste products that … Read more

Foods are the primary source that affects the functioning of kidneys. So, stop consuming these foods to protect your kidneys from harmful effects like diseases.

Dog chronic kidney disease stages in the IRIS system help vets offer better treatment to pets. Learn what each stage means. Read More!

Kidney 101 - With PKD Connect, no one will ever face polycystic kidney disease alone. Because patients, family and loved ones will always be connected to others who understand firsthand what you’re going through.

Overview of the digestive system—how food moves through each part of the GI tract to help break down food for energy, growth, and cell repair.

Top 7 Asanas Of Yoga For Kidney Health Problems Diseases, Yoga Poses For Kidney, Renal Health And Liver Function

In this article, you will discover how to use a specific fasting protocol with unique supplements to reduce pain and inflammation in the body.

Immunosuppressant drugs are a class of drugs that suppress, or reduce, the strength of the body’s immune system. Therapies that block parts of the immune system are sometimes given for several kinds of medical situations, including autoimmune diseases, as chemotherapy for cancer treatment they are also used to prevent organ transplant rejection, and as treatments for some severe skin conditions. While helpful, these drugs are also very powerful. You should know all you can about them if your doctor prescribes them for you. If your doctor has prescribed an immunosuppressant medication for you, here’s what to know about what these drugs do, how they work, and how they might make you feel. Corticosteroids Corticosteroids are anti-inflammatory medications that can be very effective in relieving symptoms of eczema, psoriasis and dermatitis. Corticosteroids suppress the activity of some immune cells, which can interrupt the inflammatory process and prevent itching, redness, and swelling. Types of corticosteroids creams – applied to the affected areas of the skin tablets – dosage varies, but is generally kept to the lowest dose possible injections – injecting straight into the affected joint, which prevents many of the side effects that occur with oral medication Your dermatologist determines the duration of topical corticosteroid treatment, which varies depending on factors such as the severity of flare-ups and the age of the person being treated. For severe eczema or dermatitis, topical corticosteroids may be used intermittently for months or years. Continued use requires regular evaluation by your dermatologist. Your healthcare provider may also prescribe medicines in severe cases. The following are commonly used to treat atopic dermatitis: Antihistamines. These medicines are taken by mouth. They may help to ease itching. Some examples include diphenhydramine and hydroxyzine. They may cause drowsiness. Steroid creams. These are put on the skin to help ease inflammation, itching, and swelling. Many topical steroids are available in various strengths. If overused, they can cause skin thinning and discoloration. Systemic corticosteroids. These medicines ease inflammation, which can relieve itching. They are used for severe cases. They are available as a pill, liquid, or shot. These steroids have serious side effects from the long-term use. So, they are only used for a short time to stop a flare-up. Oral antibiotics. These medicines kill bacteria that cause infections. Scratching the affected skin can bring bacteria to the area. This can lead to infection. Always take the antibiotic exactly as prescribed until it is all gone. Oral cyclosporine. This medicine has been used for years to treat atopic dermatitis that doesn’t respond to other treatments. It’s available as a capsule or liquid. It has many side effects that should be considered carefully. Phototherapy. Two types are used to treat atopic dermatitis: ultraviolet (UV) light therapy and PUVA (chemophototherapy). Light therapy uses UV light of specific wavelengths to target the immune system. It stops the responses that lead to inflammation. Phototherapy may be used along with other treatment. There are risks and benefits of light therapy. Weigh these risks with your healthcare provider. Topical immunomodulator. Also known as topical calcineurin inhibitors. They are put on the skin to change the immune response. Methotrexate. An immunosuppressive medicine that can be used to manage atopic dermatitis long term. However, it can potentially harm the liver. Barrier restoration creams. Like moisturizers, but they help repair the skin as well as provide moisture. Side Effects of Corticosteroids People treated with corticosteroids may experience unwanted side effects. Suddenly stopping the medication can also be dangerous, so continue taking your regular dose and see your doctor if you are troubled by side effects. Topical steroid withdrawal, sometimes referred to as ‘red skin syndrome’, can occur when frequently using or misusing moderate to high potency corticosteroids then stopping, either abruptly or reducing their dose too quickly. Withdrawal symptoms include swelling, redness, burning, and skin sensitivity and this starts usually within 1-2 weeks of stopping the steroid. Some of the more common side effects of cortisol-like drugs include: thin skin susceptibility to bruising high or increased blood pressure susceptibility to infections build-up of fat around the face, chest and abdomen osteoporosis (thinning of the bones) leading to bone fractures, particularly in the spine fluid retention (oedema) diabetes. Topical Calcineurin Inhibitors Topical calcineurin inhibitors are a type of immunosuppressant medication. They are formulated to block an overactive immune system response to the skin, which may reduce itching, redness, and swelling. Doctors typically prescribe calcineurin inhibitors when topical corticosteroids are ineffective or if eczema or dermatitis affects sensitive areas of skin that can’t be treated with topical corticosteroids for long periods. There are two types available: tacrolimus ointment (Protopic) for moderate to severe eczema and pimecrolimus cream (Elidel) for mild to moderate eczema. Topical calcineurin inhibitors generally have fewer long-term side effects than corticosteroids and may be used safely for months or years. Side effects may include a small risk of infection, and some people may experience a stinging sensation when the medication is first applied, but it generally fades over time. What are the side effects of TCIs? Clinical trials involving TCIs have looked into potential side effects, and research is ongoing to assess the long-term side effects of this relatively new treatment. The main short-term side effects identified are an irritating, burning and itching feeling on the skin where TCIs are applied. This is estimated to occur in half of all people using them. These symptoms generally disappear within a week of use. Other side effects include changes in skin colouration (skin becoming red or darker) on the area of application, a sensation of warmth on the area of application, and ‘pins and needles’. A few people also experienced blocked skin pores (folliculitis) and viral skin infections such as cold sores and warts. In children, impetigo is more common in children using TCIs. Some people experience increased skin irritation and facial flushing during tacrolimus treatment. Janus Kinase Inhibitors Janus kinase inhibitors have shown beneficial effects in a variety of immune-mediated conditions affecting the skin, joints, and gastrointestinal tract As Janus kinase inhibitors are small molecules they can be used topically or orally. Janus kinase inhibitors are used for the treatment of: Atopic dermatitis Alopecia areata Vitiligo Plaque psoriasis Other dermatoses Side effects of Janus kinase inhibitors As Janus kinase inhibitors alter the immune response, they may be associated with increased risk of serious bacterial, fungal, mycobacterial, and viral infections. Common adverse side effects of JAK inhibitors include: Nasopharyngitis Infection of upper respiratory and urinary tracts Headache Nausea and diarrhoea Immunosuppressant Overview Side effects vary greatly for the many different immunosuppressant drugs available. To find out the side affects you may be at risk for, ask your doctor or pharmacist about the effects of your particular drug. All immunosuppressant drugs carry the serious risk of infection. When an immunosuppressant drug weakens your immune system, your body becomes less resistant to infection. That means they make you more likely to get infections. It also means that any infections get will be harder to treat. If you have any of these symptoms of infection, call your doctor right away: fever or chills pain in the side of your lower back trouble urinating pain while urinating frequent urination unusual tiredness or weakness Warnings Immunosuppressant drugs can cause problems for people with certain health conditions. Tell your doctor if you have any of these conditions before you start to take immunosuppressants: allergy to the specific drug history of shingles or chickenpox kidney or liver disease Please be aware that Elidel and Tacrolimus are classed as immunosuppressants. Immunosuppressants suppress your immune response to an issue, so it is still possible to rebound from these creams. Please read about the FDA's Black-box warning for these medications here. If you need topical steroid usage support or help with steroid withdrawals you can sign up to Holistic Coaching with Kiri as she has extensive knowledge on oral and topical steroid withdrawals. And there are also steroid withdrawals support groups via ITSAN. DUPIXENT is a new injection medication. Dupixent works with your body's immune system to help reduce inflammation contributing to your eczema, which may help reduce your uncontrolled moderate-to-severe eczema (atopic dermatitis) symptoms and may give you noticeably clearer skin. Mild side effects that have been reported with Dupixent include: joint pain* reactions at the injection site, such as pain and swelling. cold sores on the lips and around the mouth. throat pain or soreness. high levels of white blood cells called eosinophils insomnia (difficulty sleeping) toothache. DUPIXENT can cause serious side effects, including: Allergic reactions. Dupixent can cause allergic reactions that can sometimes be severe. Stop using Dupixent and tell your healthcare provider or get emergency help right away if you get any of the following signs or symptoms: breathing problems or wheezing fast pulse fever general ill feeling swollen lymph nodes swelling of the face, lips, mouth, tongue, or throat hives itching nausea or vomiting fainting, dizziness, feeling lightheaded joint pain skin rash cramps in your stomach-area Eye problems. Tell your healthcare provider if you have any new or worsening eye problems, including eye pain or changes in vision, such as blurred vision. Your healthcare provider may send you to an ophthalmologist for an eye exam if needed. Joint aches and pain. Joint aches and pain can happen in people who use Dupixent. Some people have had trouble walking or moving due to their joint symptoms, and in some cases needed to be hospitalized. Tell your healthcare provider about any new or worsening joint symptoms. Your healthcare provider may stop Dupixent if you develop joint symptoms. There are dupixent support groups on Facebook and online. Pregnancy and breastfeeding Some of these drugs can cause birth defects, while others carry milder risks during pregnancy and breastfeeding. In any case, if you’re planning to become pregnant, talk to your doctor before taking an immunosuppressant drug. Your doctor can tell you about the risks of the specific drug you might be taking. If you get pregnant while taking an immunosuppressant, tell your doctor right away. The AMPERNA® Skin Solution When it comes to skin health, Kiri, founder of AMPERNA®, helps many people suffering from a variety of skin & health conditions. Kiri has developed a no-nasties steroid solution for skin concern. The probiotic complex infused within AMPERNA® products supports the skin barrier, helping to protect you from aggressions such as environmental pollutants, keep your immune system in check and reduce inflammation. AMPERNA® products deliver good bacteria to your skin gently and effectively & create the perfect conditions for your skin to breathe & shine. You can book a Holistic Skin Coaching Service to discuss your skin concerns and develop a tailored plan to work towards healthy skin. References: Immunosuppressant Drugs: A Complete Overview (healthline.com) Hormones – cortisol and corticosteroids - Better Health Channel Immunosuppressants: Definition, Treatment & What Is It (clevelandclinic.org) Medication for Eczema & Dermatitis | NYU Langone Health Immunosuppressants: Uses, Side Effects, Precautions (verywellhealth.com) Eczema | Johns Hopkins Medicine Atopic Dermatitis Medications: Main Types to Know | Everyday Health Janus kinase inhibitors | DermNet NZ Topical Calcineurin Inhibitors | Eczema.org

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