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Glomerulonephritis is an inflammation of the glomerulus, a functional unit of the kidney formed by a tangle of capillaries, where blood filtration and urine formation occur, glomerulonephritis treatment in Delhi is proposed by a nephrologist in Delhi according to the severity of the disease.

Glomerulonephritis Treatment in Delhi

Glomerulonephritis may be primary or secondary, acute or chronic. The primaries settle directly into the glomerulus and are usually caused by immunological changes resulting from infections by viruses or bacteria. According to the clinical signs they present, they are given specific names. The most common is IgA nephropathy, or Berger’s disease, which is characterized by the presence of blood in the urine, high blood pressure and, in some cases, leg edema.

The secondary ones do not originate primarily in the glomerulus but are associated with diseases such as high blood pressure, diabetes, lupus erythematosus, hepatitis B and C, HIV infection, or even some medications. The most frequent causes, however, are diabetes mellitus and systemic arterial hypertension.

The characteristics and evolution of the disease vary greatly. For example, IgA nephropathy may go into spontaneous remission and only requires that the patient be kept under observation. However, there are severe cases in which the evolution of kidney disease is rapid, aggressive, and patients with the disease should be referred for dialysis or kidney transplant in Delhi.


Primary glomerulonephritis may be asymptomatic, which delays diagnosis and initiation of treatment. When they appear, symptoms vary greatly from patient to patient. These include high blood pressure (high blood pressure), eye and/or leg edema, weight gain due to fluid retention, blood loss (hematuria) and protein (proteinuria) in the urine, tiredness, feeling unwell, weakness and anemia.

In secondary glomerulonephritis, foamy urine (as a result of proteinuria) and edema are the most common symptoms.


Clinical evaluation and laboratory tests of urine and blood, including the measurement of urea and creatinine, are important for the diagnosis of possible glomerulonephritis. The diagnosis of certainty, however, depends on the outcome of renal biopsy that should only be performed when indispensable for conducting treatment.


Glomerulonephritis treatment in Delhi is proposed by a nephrologist in Delhi according to the characteristics, severity, and causes of the disease and may require or dispense the use of medications. If there is no need to prescribe them, the recommendation is to decrease protein, salt, and fluid intake and to strictly control blood pressure.

However, medications are fundamental in the treatment of underlying diseases, especially for the control of diabetes and hypertension.


  • Periodically monitor blood pressure levels and blood sugar levels. Hypertension and diabetes are major causes of secondary glomerulonephritis;
  • Strictly follow the treatment of underlying diseases that may be the cause of glomerulonephritis;
  • Avoid excessive salt intake and alcohol consumption;
  • Give well-deserved attention to strep throat, a microorganism that can cause kidney damage.
Kidney Infection (Pyelonephritis)

Kidney Infection (Pyelonephritis)

Pyelonephritis is a potentially serious infectious inflammatory disease caused by bacteria. It affects the renal parenchyma, where the urine-producing functional structures are located, and the dilated portion of the kidney (or pelvis), roughly shaped like a funnel, whose function is to facilitate the flow of urine through the ureters. so that it is stored in the bladder and then eliminated through the urethra.

Pyelonephritis or Kidney Infection Treatment in Delhi

kidney infection treatment in Delhi

In the chronic form, the kidneys gradually lose their ability to function because of an underlying disease ( high blood pressure and type 2 diabetes, for example) or repeated or poorly cured acute infections that can lead to kidney failure.


The E.coli ( Escherichia coli ), gram-negative bacteria that normally inhabit the gut, is responsible for approximately 90% of cases of kidney infection. It enters the body through the urethra, reaches the bladder, rises through the ureters and settles in one or both kidneys, compromising its functioning. Proteus, Klebsiella, Enterobacter, and Pseudomonas are other infectious agents that may be associated with disease episodes.

Although less common, the cause of pyelonephritis may be an infection with gram-positive bacteria, including Staphylococcus aureus. Coming from infectious outbreaks in other organs, this microbe can spread into the bloodstream and infect the kidneys. It is called the hematogenous pathway of disease transmission, which can spread the bacteria throughout the body causing sepsis, a very serious infectious process known in the past as “widespread infection”.


The urinary tract has defense mechanisms that prevent the proliferation of pathogenic germs. In addition, the access of microorganisms to the upper urinary tract is hampered by the continuous flow of urine, which pulls them out of the body, and by the presence of sphincters, a type of valve that closes after the urine passes outwards.

However, even then, there are some conditions that increase the risk of developing pyelonephritis. Are they:

  • Female Anatomy – More than men, women are subject to developing urinary tract infections that can affect the kidneys. To do so, it influences the size of the female urethra (3 cm), which is much shorter than the male urethra (measures around 12 cm) and is located between the vagina  and anus, a position that favors the entry of microbes especially during the sexual act;
  • Urinary tract obstruction – kidney stones, pregnancy, anatomical malformations, prolonged use of urinary catheters, benign prostate enlargement are conditions that, in addition to slowing down urine flow and complete emptying of the bladder, favor the proliferation of bacteria that may harbor in the kidneys;
  • Weakened immune system – People with HIV, hepatitis, diabetes, or using immunosuppressive drugs may have decreased ability to react against infection;
  • Vesicoureteral reflux – the return of small amounts of urine from the urinary bladder to the ureters and kidneys during urination due to the malfunction of valves in the urinary tract. Although this reflux is more frequent in childhood, it can occur in adulthood as well.
  • Diabetes, neurogenic bladder,  polycystic kidneys, recurrent cystitis are diseases that act as important risk factors for urinary tract infections.


The symptoms of pyelonephritis are similar in the acute and chronic forms of the disease. However, it is worth noting some differences. In acute illness, they soon appear. In the chronic, asymptomatic phases alternate with others in which the clinical manifestations appear only during the periods in which the infection is active. Because of this characteristic of the disease, chronic bacterial infection can cause irreversible kidney damage that progresses to severe renal failure.

In both cases, however, the most characteristic symptoms are fever, chills, sweating, nausea, vomiting, malaise; low back and pelvic pain in the abdomen and back; urgency and pain (dysuria) to urinate, sign of pus (pyuria) and blood (hematuria) in the urine, which becomes cloudy and has an unpleasant odor.


The diagnosis of pyelonephritis considers the set of symptoms, especially the occurrence of high fever, chills and low back pain, as well as the clinical examination of the patient. Laboratory tests, such as complete blood count, type I urine and antibiogram urine culture, are useful to confirm the presence of the infection, identify the infectious agent and guide the therapeutic approach.

Imaging tests – computed tomography, ultrasound, and magnetic resonance imaging – are reserved to identify structural or anatomical abnormalities in the urinary system that pose an increased risk of severe kidney disease.

It is always important to establish the differential diagnosis with diseases that may have symptoms similar to those of pyelonephritis. These include pelvic inflammatory disease, cholecystitis ( gallbladder inflammation ), appendicitis (vermiform appendix inflammation), and acute pancreatitis (inflammation of the pancreas ).


Pyelonephritis has a cure. Kidney infection treatment in Delhi with broad-spectrum antibiotics should begin as soon as the possibility of kidney infection is raised. The goal is to prevent the infectious agent from causing permanent damage to these organs or spreading the infection throughout the body, leading to multiple organ failure.

Waiting for the result of the urine culture test to identify the type of bacteria and antibiogram to know which drug is most effective in fighting it can be risky, as both take longer to complete.

Despite the delay, however, they are fundamental tests for the treatment of recurrent infections or those resistant to the initially proposed treatment.

For pain relief when urinating (dysuria) it is ideal to use painkillers. Anti-inflammatories should only be used under medical guidance, as they may aggravate the renal condition.

In general, the standard pyelonephritis treatment in Delhi is oral antibiotics for at least seven days. Depending on the characteristics and severity of the infection, intravenous medication may be required for up to 21 days. Although symptoms usually disappear within a short time, it is essential to follow the prescribed scheme until the end to prevent the recurrence of infections or for bacteria to become resistant to the indicated antibiotics.

Severe kidney infections, especially in childhood and the elderly, may require hospitalization to administer intravenous medication. Patients with chronic pyelonephritis, which leads to progressive and irreversible loss of the kidney, depending on dialysis until a kidney transplant can be performed.

Surgical procedures are indicated when obstructions or structural abnormalities of the urinary system facilitate the installation of infectious processes.


  • Drink plenty of fluids, preferably water. In addition to keeping the body well hydrated, fluids help eliminate infectious agents when the person urinates;
  • Answer your urge to empty your bladder promptly. Urine stored in the bladder can become a hotbed of infection;
  • Urinate shortly after sexual intercourse as a means of eliminating bacteria that may have penetrated the urethra;
  • Proceed to local hygiene with water. If using toilet paper after urinating or bowel movement, wipe it back and forth to prevent bacteria from spreading through the urethra and bladder.
  • Double your attention if you are pregnant. Natural changes in your body – changes in urine characteristics, accelerated the growth of the uterus and consequent bladder compression – increase the predisposition to urinary tract infections;
  • Do not self-medicate or discontinue medication without first hearing what your kidney specialist in Delhi has to say.
Malignant hypertension

Malignant Hypertension

Malignant hypertension is a disease where, in addition to high blood pressure, there is damage to specific organs (such as the kidneys). It is a situation that needs immediate care and expert judgment as there is a risk of serious organ damage such as kidneys and even death.

Malignant arterial hypertension is characterized by severe and abruptly severe blood pressure elevation (characterizing a hypertensive emergency) where there is damage to target organs (vital organs) such as the kidneys and retina with retinal hemorrhage and papilla edema (vision). It requires an immediate reduction in blood pressure in a hospital setting. It is an important cause of morbidity and mortality.

This is why it is very important that a person is known to have high blood pressure regularly follow up with a CARDIOLOGIST and Nephrologist in Delhi and do not let you take the prescribed medications.

The suspicion of renovascular hypertension is based on suggestive clinical findings, such as treatment-refractory hypertension, appearing before 20 and after 50 years, or associated with renal insufficiency.

The main complementary tests for screening for renovascular hypertension are captopril radioisotopic renal scintigraphy, peripheral renin collection captopril test, renal artery Doppler and, more recently, magnetic resonance angiography. The diagnosis is confirmed only by arteriography. Recent studies have shown alterations in endothelial function, oxidative stress and sympathetic nervous system in renovascular hypertension, which may be involved in the cardiovascular complications of these patients.

The main goals of renovascular hypertension treatment are the effective control of arterial hypertension and the preservation of renal function. The three available therapeutic modalities include clinical treatment, angioplasty or stent implantation and surgical revascularization. The choice of treatment should be individualized based on age, etiology of stenosis and the presence of associated diseases.

Malignant hypertension is a serious complication of hypertension, characterized by severe and acute elevation of blood pressure, rapidly progressive renal failure, severe retinopathy and heart failure, culminating in the patient’s death within a few months if not treated properly. Currently, better control of blood pressure with effective treatment and knowledge of new pathophysiological mechanisms have improved the survival of these patients.

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Systemic Erythomatous Lupus

Systemic Erythomatous Lupus is a chronic inflammatory disease of autoimmune origin, the symptoms of which may appear in various organs slowly and progressively (in months) or more rapidly (in weeks) and vary with phases of activity and remission.

Two main types of lupus are recognized: the cutaneous, which manifests only with patches of skin (usually reddish or erythematous and hence the name lupus erythematosus), especially in areas that are exposed to sunlight (face, ears, neck (“V Neckline) and arms) and the systemic, in which one or more internal organs are affected.

Because it is a disease of the immune system, which is responsible for antibody production and organization of inflammation mechanisms in all organs when a person has SLE they may have different types of symptoms and various body locations. Some symptoms are generally such as fever, weight loss, loss of appetite, weakness, and discouragement. Other, organ-specific such as joint pain, skin blemishes, pleural inflammation, hypertension, and / or kidney problems.

Who has lupus?

Lupus can occur in people of any age, race, and gender, but women are much more affected. It occurs mainly between 20 and 45 years, being a little more frequent in people of mixed race and Afro-descendants. In India, we do not have exact figures, but estimates indicate that there are about 65,000 people with lupus, most of them women. It is thus believed that one in 1,700 women in Brazil has the disease.

What causes lupus?

Although the cause of SEL is not known, it is known that genetic, hormonal and environmental factors play a part in its development. Therefore, people who are born with genetic susceptibility to develop the disease, at some point, after an interaction with environmental factors (solar radiation, viral infections or other microorganisms), have immunological changes.

The main one is the imbalance in the production of antibodies that react with proteins in the body itself and cause inflammation in various organs such as the skin, mucous membranes, pleura and lungs, joints, kidneys, etc.). Thus, we understand that the type of symptom that a person develops depends on the type of autoantibody that the person has and that how the development of each antibody relates to each person’s genetic characteristics,

What are the symptoms of the disease?

The symptoms of SEL are diverse and typically vary in intensity according to the phase of activity or remission of the disease. It is very common for the person to have general manifestations such as tiredness, discouragement, low fever (but rarely, maybe high), weight loss and loss of appetite.

Manifestations may occur due to inflammation in the skin, joints (joints), kidneys, nerves, brain and membranes covering the lung (pleura) and heart (pericardium). Other manifestations may occur due to decreased blood cells (red and white blood cells) due to antibodies against these cells. These symptoms may arise in isolation or together and may occur simultaneously or sequentially. Children, adolescents or even adults may have swollen ganglia,

The most frequent clinical manifestations are:

Skin lesions: occur in about 80% of cases, throughout the course of the disease. The most characteristic lesions are reddish patches on the cheekbones and back of the nose, called butterfly wing lesions (the distribution on the face resembles a butterfly) and leave no scar.

Discoid lesions, which also occur more frequently in areas exposed to light, are well delimited and can leave scars with atrophy and changes in skin color. Vasculitis (inflammation of small vessels) can also occur on the skin, causing painful red or wine spots on the fingertips or toes.

Another very characteristic manifestation in SEL is what is called photosensitivity, which is nothing more than the development of a disproportionate sensitivity to sunlight. In this case, With only a little exposure to light or sun, it may result in skin blemishes as well as general symptoms (tiredness) or fever. Hair loss is very common but typically occurs in the activity stages of the disease and in most people hair usually regrow with treatment.

Articular: Joint pain with or without joint swelling occurs at some point in over 90% of people with SEL and mainly involves the joints of the hands, wrists, knees, and feet, which tend to be quite painful and occur in a way that occurs. intermittent, with periods of improvement and worsening. Sometimes they also arise as tendonitis.

Inflammation of the membranes covering the lung and heart is relatively common and may be mild and asymptomatic, or manifest as chest pain. Characteristically in the case of lung, pain occurs when breathing and may also cause a dry cough and shortness of breath. In pericarditis, in addition to chest pain, there may be palpitations and shortness of breath.

Kidney inflammation (nephritis): is one of the most worrying and occurs in about 50% of people with SEL. At first, there may not be any symptoms, only changes in blood and/or urine tests. In the most severe forms, high blood pressure, swelling in the legs, urine becomes foamy and there may be a decrease in the amount of urine. When not treated promptly and properly the kidney fails (kidney failure) and the patient may need dialysis or kidney transplantation.

Neuropsychiatric disorders: These manifestations are less frequent, but may cause seizures, mood or behavior changes (depression), depression, and peripheral nerve and spinal cord changes.

Blood: Changes in blood cells are due to antibodies against these cells, causing their destruction. Thus, if antibodies against red blood cells (RBCs) will cause anemia, against white blood cells will cause decreased white cells (leukopenia or lymphopenia) and if against platelets will cause decreased platelets (thrombocytopenia).

Symptoms caused by changes in blood cells vary widely. Anemia can cause pale skin and mucous membranes and tiredness, and thrombocytopenia can cause increased menstrual bleeding, bruising and gum bleeding. Usually, the decrease in white blood cells is asymptomatic.

How is the diagnosis made?

The diagnosis is made by the doctor recognizing one or more of the above symptoms. At the same time, as some changes in blood and urine tests are very characteristic, they are also commonly used for the final definition of the diagnosis. Common blood and urine tests are useful not only for the diagnosis of the disease but are also very important in defining whether there is SLE activity.

Although there is no test that is exclusively for SEL (100% specific), the presence of the test called ANF (antinuclear factor or antibody), especially with high titers, in a person with signs and symptoms characteristic of SEL, allows the diagnosis with much assurance.

Other laboratory tests such as anti-Sm and anti-DNA antibodies are very specific but occur in only 40% to 50% of people with SEL. At the same time, some blood and/or urine tests may be ordered to assist not in diagnosing SEL but in identifying whether or not there are signs of disease activity.

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Chronic Renal Insufficiency

Chronic Renal Failure Treatment in Delhi

Chronic Renal Failure Treatment in Delhi

It consists of the progressive and irreversible deterioration of renal function. When the glomerular filtration rate – blood filtering in the kidney – falls below 25 to 35%, urea and creatinine begin to increase, patients being relatively asymptomatic or presenting anemia, high blood pressure, polyuria, and nocturia. When glomerular filtration falls below approximately 15%, signs of uremic syndrome begin to appear and require urgent chronic renal failure treatment in Delhi.


Diabetes mellitus: the most frequent cause of CRF in developed countries. Renal involvement occurs after 10 years of diabetes, although it manifests clinically at 20 years.

Hypertension: produces an overload of pressure in the entire vascular tree, to which the vessels respond by strengthening their muscular layer. In the kidney there is a thickening of the wall of the vessels with a decrease in their caliber, leading to renal ischemia, and, on the other hand, glomerular hypertension occurs that puts excessive work on the glomerulus.

Glomerulonephritis: they consist of a glomerular involvement accompanied by vascular and renal interstitial involvement in some cases. Clinically they usually manifest with proteinuria, hematuria and slow or rapid deterioration of renal function (from days to years).

Tubulointerstitial nephritis: processes that predominantly affect the interstitium – one of the kidney areas – with the destruction of tubules and vessels, which results in ischemia and renal atrophy.

Hereditary renal processes: represented almost entirely by polycystic kidney disease. It is a hereditary process that is transmitted in an autosomal dominant manner and is a defect in the formation of renal tubules, which degenerate into cysts that grow progressively and destroy the healthy renal parenchyma.


Electrolyte disorders: abnormalities occur in the levels of different electrolytes such as potassium and bicarbonate. These alterations occur in advanced stages of renal failure. Other abnormalities such as hypocalcemia and hyperphosphatemia may appear when renal failure is moderate.

Cardiovascular manifestations: arterial hypertension, found in up to 80% of patients with end-stage chronic renal failure. The fundamental cause is hydro saline retention, although a hyperreninemia situation is also involved.

Gastrointestinal disorders: anorexia, nausea, and vomiting. A characteristic sign is a uremic fever, ammoniacal smell produced by nitrogen metabolites in saliva.

Hematological disorders: an early sign in the evolution of chronic renal failure is anemia, largely caused by erythropoietin deficiency (hormone synthesized in the kidney and that promotes the generation of red blood cells), although other factors such as gastric losses also influence, decreased half-life of red blood cells due to the same uremia, malnutrition or iron deficit.

Neurological disorders: the appearance of uremic encephalopathy is typical, which manifests itself as a cognitive disorder that ranges from difficulty concentrating to deep coma. A polyneuropathy may also appear that is sensitive at first but that, if it advances, also becomes motor.

Osteomuscular disorders (renal osteodystrophy): it is manifested by bone pain, deformities (resorption of distal phalanges in fingers), fractures and growth retardation in children.

Dermatological alterations: the characteristic sign is the straw color of the skin, produced by anemia and the accumulation of urochromes. Itching (itching) is also very frequent and very annoying.

Hormonal alterations: in man it mainly causes impotence and oligospermia (decrease in sperm production). In women, it causes alterations in the menstrual cycle and often amenorrhea (lack of menstruation).


The diagnosis of chronic renal failure is based on the clinical manifestations presented by the patient, as well as the alterations that can be seen in blood tests.

The ultrasound shows that the kidney has decreased in size and has an alteration in its usual structure.

Conservative Treatment

It is important to start the chronic renal failure treatment in Delhi early in order to avoid complications, anticipate long-term sequelae and slow the progression of the disease as much as possible (protecting residual renal function).

Dietary control:
  • Restriction of the consumption of salt, proteins, foods rich in phosphorus and potassium.


  • Protectors of renal function: angiotensin-converting enzyme inhibitors.

Electrolytic Correctors:

  • Chelants of phosphorus.
  • Potassium chelators are used in very terminal phases of chronic renal failure.

Hormonal correctors:

  • Vitamin D: helps control the increase in parathyroid hormone and promotes calcium absorption and bone mineralization.
  • Erythropoietin: stimulates the production of red series cells.

Substitute Treatment

There are currently three treatments for chronic end-stage renal failure: hemodialysis, peritoneal dialysis, and kidney transplant in Delhi.

In hemodialysis, the elimination of toxins and excess liquid is done through an artificial filter. It requires an extracorporeal circuit with the need for vascular access (arteriovenous fistula or hemodialysis catheter). It consists of intermittent sessions (three a week) of variable duration (3 to 4 hours).

In peritoneal dialysis, the elimination of toxins and fluid occurs through the membrane of the peritoneum. It requires a complete peritoneal cavity in need of implantation of a peritoneal dialysis catheter to introduce dialysis fluid into the abdomen. It is continuous dialysis, requiring the replacement of peritoneal dialysis fluid three or four times a day.

Transplant :

The steps followed in performing a transplant are as follows:
  • Donor corpse.
  • Compatibility of blood and immune group.
  • Receptor selection (age, time on dialysis, clinical situation).
  • Receiver Preparation
  • Surgery.
  • Immediate postoperative control (ICU).
  • Late postoperative control (plant).
  • Follow up in consultation.