Table of Contents

1. Functions of Kidneys
2. Kidney Disease and its Risk Factors
3. National Kidney Month and Free Screenings
4. Anatomy and Physiology of Kidneys
5. Roles of Kidneys in the Body
6. Causes and Types of Kidney Diseases
7. Acute Kidney Injury (AKI)
8. Manifestation of Kidney Diseases
9. Diagnosis of Kidney Diseases
10. Conclusion


Kidneys are the body’s chemical factories, filtering waste and performing vital functions that control red blood cell production and blood pressure. 1 in 9 American adults has kidney disease.

Kidney disease risk can be addressed to a great extent by controlling blood pressure and blood sugar, quitting smoking, regular exercise, maintaining a healthy weight, and avoiding excessive use of pain medications. Early detection and treatment can slow or prevent the progression of kidney disease. A wide range of other organ systems disease may be manifested in the kidney (1). For example, renal disease is a prominent presentation of long-standing diabetes mellitus and hypertension and of autoimmune disorders such as systemic lupus erythematosus.


Joseph Vassalotti, MD, National Kidney Foundation Chief Medical Officer says “Of the 26 million American adults estimated to have kidney disease, most don’t know they have it”. The National Kidney Foundation, leading organization in the U.S. dedicated MARCH month for spreading the awareness of kidney disease and offers free screenings to those most at risk for kidney disease. March is the National Kidney Month and is a perfect time to learn more about how to keep kidneys healthy.

There are two kidneys in the human body, each about the size of fist located near the middle of the back, just below the rib cage. Each kidney has about a million tiny structures called nephrons which filter blood with the help of glomerulus and tubule. The two-step process is glomerulus filters blood, and the tubule returns needed substances to blood and removes wastes. Kidneys perform a plethora of functions by filtering 200 liters blood/day, removing two liters of toxins and wastes.

The kidneys play multiple roles in the body, including blood filtration, metabolism, and excretion of endogenous and exogenous compounds, and endocrine functions. It regulates the body’s hydration and water balance, blood pressure by controlling fluid levels, keep blood minerals in balance, keep electrolytes in balance, regulate blood acid levels, remove certain drugs from the blood, eliminate excess water-soluble vitamins. The wastes and extra water is excreted which become urine flowing through tubes called ureters it goes to the bladder, which stores the urine and removes out of the body. Perhaps most significantly, the kidneys are the primary regulators of fluid, acid-base, and electrolyte balance in the body, and this remarkable pair of organs maintain homeostasis across a broad array of dietary and environmental changes. In order to illuminate the pathophysiologic basis behind the many different manifestations of kidney disease, an understanding of each of these roles is required.

Most of the kidney diseases attack the nephrons and due to which kidneys become unable to remove wastes. The damage to the kidneys can occur due to genetic problems, injuries, or medicines. Risk of kidney disease increases in diabetes, high blood pressure, or in hereditary defects. However, hereditary defects account for a minority of glomerular disease. Over the counter pain medicines, such as NSAIDs (nonsteroidal anti-inflammatory drugs), harm the kidneys, especially in patients with kidney disease.

Acute kidney injury (AKI) is responsible for approximately 2 million deaths annually worldwide. It represents an independent cardiovascular risk factor for mortality in hospitalized patients especially in those on renal replacement therapy (RRT) (3). First of all, oliguria can lead to sodium and water retention with consequent fluid overload and development of edema, cardiac overload, hypertension, pulmonary edema, and myocardial injury. Furthermore, electrolytes imbalance can contribute to the raised risk of fatal arrhythmias and sudden death. Patients with the most severe form of AKI who require renal replacement therapy have a mortality rate of 50–80%. In the chronic kidney, disease nephrons get damaged slowly over several years. Other kidney problems include cancer, cysts, stones, and infections. Renal tissue gets exposed to a significant quantity of any potentially harmful circulating agents or substances due to the rate of renal blood flow which is 400 ml/100g of tissue per minute. This is much greater than that observed in the heart, liver, and brain. The glomerular capillaries are vulnerable to hemodynamic injury due to high intra and trans glomerular pressure. Glomerular hypertension and hyperfiltration have been identified as major contributors to the progression of chronic renal disease. There is an electrostatic barrier at glomerular filtration membrane and with disruption in its plasma protein gains access to the glomerular filtrate. Unfortunately, it takes a long time to realize if kidneys are malfunctioning.

Kidney disease usually doesn’t surface and patient don’t feel sick until the problem becomes serious and irreversible. The different types of kidney diseases harm the tiny filters called nephrons and reduce their filtering ability. When damage to nephrons happens quickly it is known as acute kidney injury. There are no pain receptors within the substance of the kidney. Therefore pain is not a prominent presenting complaint, except in patients with renal diseases (eg, nephrolithiasis) in which there is involvement of the ureter or the renal capsule.

Early stages of kidney disease are marked by abnormalities of urine volume (eg, oliguria) or composition (eg, the presence of red blood cells and/or protein). Hence, a particular challenge is that patients are typically asymptomatic until relatively advanced kidney failure is present. The manifestation of systemic symptoms and signs of lost renal function occurs later (eg, edema, fluid overload, electrolyte abnormalities, and anemia). The urine test checks for a protein called albumin, and the blood test checks GFR – glomerular filtration rate, which is an estimate of the kidney’s filtering ability. A GFR below 60 is indicative of chronic kidney disease whereas below 15 is described as kidney failure. According to studies, the main causes of renal injury are based on immunologic reactions (initiated by immune complexes or immune cells), tissue hypoxia and ischemia, exogenic agents like drugs, endogenous substances like glucose or paraproteins and others, and genetic defects. Irrespective of the underlying cause glomerulosclerosis and tubulointerstitial fibrosis are common to the chronic condition (2). The diseases are broadly divided into three groups. The first group is nonproliferative glomerular diseases with deposition of immunoglobulins, without glomerular inflammation, most likely because of subepithelial localization of immunoglobulins (e.g., membranous nephropathy). The podocyte seems to occupy the central role in the pathogenesis. The second group is proliferative glomerular diseases with deposition of immunoglobulins leading to increased cellularity resulting in inflammatory cell recruitment, or with severe glomerular injury and inflammation, but without deposition of immunoglobulins. The offending etiologic agents are mainly unknown, with the rare exception of ß hemolytic streptococci in post-streptococcal glomerulonephritis, and hepatitis C virus in type 1 cryoglobulinemic membranoproliferative glomerulonephritis. Reactive oxygen species, protease, cytokines, chemokines and other inflammatory mediators originating from recruited and resident inflammatory cells play the key pathogenic roles. TGF-ß and connective tissue growth factor (CTGF) are important in glomerular fibrogenesis, and they are involved in stimulating glomerular cells to produce extracellular matrix (ECM), a key event in the progression of kidney disease. ECM inhibits the synthesis of tissue protease, mostly matrix metalloproteinase, which otherwise degrades matrix proteins. Glomerular inflammation gets resolved with a variable degree of fibrosis or recovers completely. The resolution process demands the cessation of antibodies production and immune complex formation, cessation of recruitment and clearing of inflammatory cells, dispersing of inflammatory mediators, normalization of endothelial adhesiveness, permeability, and vascular tone, and clearance of proliferating resident glomerular cells. Also, the degradation and removal of deposited and circulating immune complexes are required.


Dialysis is a treatment which allows patients with kidney failure to feel better and continue with everyday activities. This process filters wastes and water from the blood. A healthy lifestyle, including physical activity and a heart-healthy diet, can help to normalize blood pressure and also slow kidney disease. Researchers are exploring innovative ways to improve the quality of life and long-term outcome for these patients.