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1. Introduction
The prevalence of kidney diseases has increased globally and continues to rise. However, kidneys are organs that play an important role in metabolic activities. The absorption of minerals and water, acid-base balance, and the functionality of buffer systems are regulated by the kidney and are of vital importance [1]. The proteasuria, membranous nephropathy, diabetic nephropathy, complement-mediated-kidney-disease, and other kidney pathologies examined by eminent authors in this book with the aim of opening new horizons. I hope the content of our book will be useful to dear readers.
2. Nephritis
Nephritis is a condition in which the nephrons, the functional units of the kidneys, become inflamed. This inflammation, or glomerulonephritis, can negatively affect kidney function [2].
When the kidneys function normally, the rest of the body is constantly supplied with oxygen-rich blood. However, when the kidneys become inflamed, they cannot filter the blood effectively. The kidneys are the filters of the body. These two bean-shaped organs are a special evacuation system. It processes almost 150 L of blood every day and disposes of up to 2 L of useless residue and water. Acute nephritis occurs when the kidneys become rapidly inflamed, this inflammation causes kidney dysfunction. Acute nephritis has many causes and if left untreated, kidney failure occurs [3].
Although the disease has an acute and chronic course, there are several forms attributed to nephritis:
2.1 Interstitial nephritis
Spaces between kidney tubules to inflammation are called interstitial nephritis. It can be acute or chronic, acute interstitial nephritis is considered a disease characterized by a decline in renal functions, inflammatory infiltrate in the interstitium, and inflammatory edema. It is the second most common cause of intrinsic kidney disease [4].
It is now thought that almost all drugs can cause acute interstitial nephritis, and drugs are responsible for 60–70% of acute interstitial nephritis cases. The disease can be idiopathic, as well as infections, and systemic lupus, except for drugs. Systemic diseases such as erythematosus and sarcoidosis may also be associated with malignancy. Antibiotics are the group of drugs that most commonly cause acute interstitial nephritis. However, it has been understood that proton pump inhibitors are the second most common drug group in patients over 65 years of age, and nonsteroidal anti-inflammatory drugs are the second most common drug group in patients under 65 years of age [5].
2.2 Pyelonephritis
Pyelonephritis usually occurs as a result of inflammation of the kidney by bacterial infections. In most cases, the infection begins in the bladder, spreads to the ureters, and finally reaches the kidneys [6].
Individuals with recurrent febrile urinary tract infections develop a kidney injury, high pulse, extreme changes in renal function, and then renal failure. The frequency of urinary tract diseases changes depending on age, gender, and diagnostic methods used. According to the American Academy of Pediatrics, the prevalence in children under two years of age with fever is over 5% [7]. For all age groups, it occurs at a rate of 3–5% in girls and 1% in boys. Although all kinds of microorganisms (fungi, parasites, and viruses) that can colonize the urinary system can cause urinary tract infections, the most common factor is gram (−) enteric bacteria. In this group,
2.3 Glomerulonephritis
Glomerulonephritis is one of the most common renal disorders. Recently, it has been the third cause of kidney diseases in our country after diabetes mellitus (DM) and hypertension in 2010 records [9].
Glomerulonephritis (GN) is defined as an acute or chronic inflammation of the glomerulus. The capillary endothelium, mesenchyme and basement membrane compartments that form the basis of the glomerulus may be affected by this inflammation [10].
Acute glomerulonephritis (AGN) is a clinical picture and nephritic disorder characterized by the sudden onset of macroscopic hematuria, proteinuria at different levels, azotemia, oliguria, edema, and hypertension-like symptoms and findings [2, 3, 4]. Mostly antigen-antibody reaction is the factor initiating the immunological period. The causes of tissue destruction, increased vascular permeability, and glomerular inflammation that occur in this period are the activation of one or more of the inflammatory mediator systems such as complement system, cytokines, coagulation, and growth factors. Glomerular filtration rate (GFR) decreases abruptly due to inflammation and edema in the glomeruli with a change in tissue blood supply. Oliguria, edema, azotemia, hypertension, and damage to endothelial cells result in the retention of water and metabolic products in the urine, resulting in proteinuria and hematuria. The clinical picture varies according to the degree of volume excess. Life-threatening clinical findings such as severe pulmonary edema and hypertension may occur in case of severe volume overload [11].
3. Diagnosis
The most common symptoms are pain in the pelvic area, on urination or burning sensation in the penis, need to urinate more frequently, cloudy urine, presence of blood or pus in the urine, swelling of the face, legs, and feet, vomiting, fever, and high blood pressure [12].
In addition to the aforementioned physical findings, the presence of an infection in laboratory tests, and the presence of bacteria and white blood cells (WBC) in urinalysis are important. Elevated blood urea nitrogen (BUN) and creatinine levels in blood tests are important parameters used in the detection of the disease. Imaging techniques such as a CT scan or kidney ultrasound can show blockage or inflammation of the kidneys or urinary tract. A kidney biopsy is also one of the best ways to diagnose nephritis. The metabolic effects of impaired kidney function are monitored by changes in blood biochemistry.
Possible biochemical differences in the case of AGN in the patient are decreased serum sodium and calcium levels, metabolic acidosis, and increased levels of phosphorus, potassium, magnesium, uric acid, urea, and creatinine in blood serum [13].
There may be anemia of dilutional character. It is understood that plasma renin activity is suppressed in proportion to the severity of fluid retention [14].
Macroscopic hematuria, proteinuria, hypertension, and acute renal failure are common in hemolytic uremic syndrome, but thrombocytopenia and anemia are also seen. Diarrhea may be seen in HUS. Proteinuria and macroscopic hematuria occur; hearing loss, family history and renal biopsy will enable the diagnosis in some patients with Alport syndrome [11, 12].
4. Nephrotic syndrome and nephrosis
Nephrotic syndrome (NS) is a clinical picture characterized by massive proteinuria resulting from increased permeability of the glomerular filtration barrier and resulting in hypoproteinemia, edema, and hyperlipidemia. The annual incidence of NS is reported to be 2.0–2.7 per 100.000 in children under 16 years of age, with a male-to-female ratio of 2/1 in childhood, equal in adulthood and adolescence, and more common in blacks than whites.
In childhood, 2/3 of NSs start before the age of 5 years and 80–85% are caused by minimal change disease(MCD) [15].
is classified according to clinical appearance, histopathological lesion, and response to steroid treatment.
4.1 Clinical classification
(NS) is analyzed in two main groups primary and secondary NS according to its formation.
In primary NS, the event is isolated in the kidney and the most common type is MCD, which responds well to steroids. Non-MCD glomerulonephritis also responds to steroids at a lower rate than MCD [16].
Primary NS consists of idiopathic NS [MCD, focal segmental glomerulosclerosis (FSGS), mesengioproliferative glomerulonephritis (MesPGN)], MGN, immunocomplex glomerulonephritis [acute poststreptoxic glomerulonephritis (APSGN), membranoproliferative glomerulonephritis (MPGN)], and congenital NS. Secondary NS develops secondary to a systemic disease or event [16, 17].
Clinical Classification of (NS):
4.1.1 Primary NS
Idiopathic NS
Minimal change disease (MCD)
Mesangial proliferative glomerulonephritis (MesPGN)
Focal glomerulosclerosis (FGS)
Immunocomplex glomerulonephritis
Membranous glomerulonephritis (MGN)
Membranoproliferative glomerulonephritis (MPGN)
Acute post-streptococcal glomerulonephritis (APSGN)
Congenital NS
4.1.2 Secondary NS
Systemic diseases: Henoch-Schönlein purpura, systemic lupus erythematosus (SLE), vasculitis, Goodpasture syndrome, dermatomyositis, amyloidosis, sarcoidosis, and rheumatoid arthritis.
Systemic infections: Hepatitis B, congenital and secondary syphilis, shunt infection, bacterial endocarditis, malaria, varicella, HIV, post-steroptotoxic glomerulonephritis, leprosy, schistosomiasis, and infectious mononucleosis.
Heredofamilial diseases: Sickle cell anemia, diabetes mellitus, Alport syndrome, and nail-patella syndrome.
Drugs: Gold salts, nonsteroidal anti-inflammatory drugs (NSAIDs), tridione, captopril, heroin, d-penicillamine, and mercury compounds.
Neoplasms: Hodgkin’s disease, lymphomas, leukemias, carcinomas, melanomas, and Wilms’ tumor.
Others: Bee sting, vaccination, thyroiditis, myxedema, and malignant obesity.
4.2 Histopathological classification
It is made according to the glomerular changes seen in light microscopy. This distinction was later supported by immunofluorescence and electron microscopic examinations [18].
Histopathological Classification of Glomerular Lesions
Minimal Change Disease (MCD)
Focal Glomerulosclerosis (FGS)
Focal Segmental Glomerulosclerosis (FSGS)
Focal Global Glomerulosclerosis (FGGS)
Mesengial Proliferative Glomerulonephritis(MesPGN)
Pure Diffuse Mesangial Proliferation
Sclerosing Glomerulonephritis
Membrano-Proliferative Glomerulonephritis (MPGN)
Type-I MPGN; Subendothelial storage
Type-II MPGN; Intramembranous dense deposits
Type-III MPGN; Transmembranous storage
Membranous Glomerulonephritis (MGN)
Chronic Glomerulonephritis
4.2.1 Minimal change disease
In minimal lesion disease, it is accepted that there is no histological change in glomeruli. In some cases, minimal mesangial thickening, focal mesangial cell increase, and thickening of the basement membrane may be seen. Immunofluorescence microscopy usually shows no immuno-deposit deposition. However, mesangial deposition consisting of IgM and complement may be found, although rarely. Electron microscopy shows hypertrophy of podocytes and enlargement of foot processes. In childhood, 2/3 of NSs start before the age of 5 years and 80–85% are caused by MCD [15, 19].
(NS) is classified according to clinical appearance, histopathological lesion, and response to steroid treatment. The annual incidence of NS is 2.0–2.7 per 100,000 in children under the age of 16, the male-female ratio is 2/1 in childhood, it is equal in adults and adolescents, and it is more common in the black race than white [20, 21].
4.2.2 Focal glomerulosclerosis
In focal glomerulosclerosis (FGS), some glomeruli show increased matrix and hyaline deposition with segmental areas of capillary collapse and obliteration (FSGS). There may be widespread involvement [focal global glomerulosclerosis (FGGS)]. In most lesions, podocyte hyperplasia is accompanied by sclerotic areas. The affected glomeruli are often in the juxtamedullary region but are not limited there. FGGS may be an advanced form of FSGS or an independent entity unrelated to NS. As a rule, FSGS is accompanied by tubular atrophy and responds to steroids worse than MCD but better than FGGS. It has a progressive course [18, 22, 23].
4.2.3 Mesengial proliferative glomerulonephritis
Mesengioproliferative glomerulonephritis is characterized by a moderate to a marked increase in the number of mesengial cells (mesengial proliferation), leukocyte infiltration (exudation), and increased mesengial matrix (sclerosis) with obliteration of capillary loops and fibroepithelial proliferation (crescent and adhesion) on the inner surface of Bowman’s capsule. Immunofluorescence microscopy is usually negative. However, NS findings secondary to postinfectious glomerulonephritis, Berger’s disease (IgA nephropathy), and systemic disease may be present [18, 22].
4.2.4 Membrano-proliferative glomerulonephritis
Three histological subgroups have been defined under the title of membranoproliferative glomerulonephritis (MPGN). In Type-I MPGN, the main lesion is subendothelial IgG and complement deposition. In Type-II MPGN there is basement membrane thickening with intramembranous dense storage. Type-III MPGN is morphologically characterized by transmembranous deposition. Mesangial proliferation, crescent formation, hyperlobulation, and epimembranous deposition are observed in all types [18, 22, 24].
4.2.5 Membranous glomerulonephritis
In membranous glomerulonephritis, subendothelial deposits are usually regularly, sometimes irregularly distributed in the basement membrane. In light microscopy, they are seen as basement membrane protrusions indenting the lamina densa. This appearance is described as a lace-like appearance. Deposits are usually associated with only mild mesangial proliferation [25, 26].
4.2.6 Chronic glomerulonephritis
Most types of acute glomerulonephritis are susceptible to transformation into chronic glomerulonephritis. This condition causes progressive glomerular and tubulointerstitial fibrosis. There is an irreversible progressive decrease in glomerular filtration rate. Uremic toxins accumulate in the blood and lead to disease progression, resulting in chronic kidney disease (CKD), end-stage renal disease (ESRD), and cardiovascular disease. Chronic glomerulonephritis is a leading cause of chronic kidney disease and accounts for approximately 10% of all patients on dialysis [27].
4.3 Pathophysiology of (NS)
Proteinuria, which occurs with increased permeability in the filtration barrier, is the primary pathophysiological mechanism responsible for the development of NS. The protein most lost in urine is albumin, but other plasma proteins such as immunoglobulins, various coagulation factors, vitamin-D binding proteins, and metalloproteins are also lost in urine [15, 19]. Albuminuria causes edema, hypoalbuminemia and hypercholesterolemia in patients [28].
4.3.1 Proteinuria
Protein excretion of more than 40 mg/m2/st in children and more than 3.5 g/day in adults is considered nephrotic proteinuria [18].
Normally, large molecular weight proteins are not seen in the urine due to the selective permeability of the glomerular filtration barrier and reabsorption of proteins from the proximal tubulus. In glomerular diseases, increased glomerular permeability to proteins results in proteinuria. Despite extensive research, the pathogenesis of proteinuria is still not fully explained. In filtration function, glomerular basement membrane (GBM) functions as a barrier based on both molar size and electrical charge, and epithelial cells, the outermost layer of the glomerular capillary network, acts as a selective barrier for the filtration of micromolecules. Visceral epithelial cells (podocytes) form the outermost part of the glomerular filtration barrier. Podocytes surround the glomerular capillaries in the form of scallop teeth. Each comb tooth is formed by neighboring epithelial cell peduncles. Peduncular outgrowths are associated with GBM. Between the neighboring adaxial processes on the GBM is the slit diaphragm (SD), a bridge containing filtration holes. The slit diaphragm is a very thin membrane closely associated with the GBM. Glycoproteins, predominantly podocalyxin, cover the apical and lateral surfaces of the peduncular processes. These structures cause the foot processes to carry a strong negative electric charge. The negative electric charge also prevents the adhesion of neighboring peduncles to each other [18].
4.3.2 Definition of normal and nephrotic proteinuria
Qualitative
Presence of 1+ (30 mg/dl) protein by dipstick method in two of three urine samples with density below 1015.
Presence of 2+ (100 mg/dl) protein in urine samples with a density above 1015.
Semiquantitative; protein/creatinine ratio in morning urine (mg/mg)
Normal below 0.2
0.2–2.0 light
Severe proteinuria above 2.0
Quantitative
Normal and nephrotic proteinuria can be evaluated according to the following classification [23]
Abnormal: 4–40 mg/m2/hr. in 12–24 hour urine samples
Nephrotic limit: > 40 mg/m2/hr. in 12–24 hour urine samples
4.3.3 Hypoalbuminemia
Hypoalbuminemia resulting from massive proteinuria is a constant laboratory finding of NS1–3. There is an inverse relationship between urinary protein loss and serum albumin level. However, this is not always valid. In children with prolonged proteinuria unresponsive to treatment, serum albumin levels may be normal or near normal without any change in protein excretion rate. The hepatic albumin synthesis rate may be normal or increased in NS [29].
The severity of hypoalbuminemia varies from patient to patient. The serum albumin level during relapse varies between 0.5 g/dl and 2.5 g/dl [18, 22].
Other protein abnormalities in plasma include decreased gamma-globulin, normal or low alpha1-globulin, alpha2-globulin, and increased fibrinogen levels. The increase in alpha2-globulin level is thought to be due to accumulation. In patients with NS, especially MCD, IgG level decreases while IgM level increases [28].
4.3.4 Edema
It is the main clinical finding of NS is classic, edema seen in NS is caused by a decrease in plasma oncotic pressure as a result of hypoalbuminemia, and secondary to this, water and solutes pass into the interstitial space. This results in a decrease in intravascular volume, which activates the renin-angiotensin-aldosterone system. As a result, water and salt retention increases (underfilling theory) [18, 22]. The observation that intravascular volume is normal or increased and plasma renin activity is not increased in some NS patients suggests that other factors may also play a role in the formation of NS edema. In these cases, sodium retention is thought to occur by intrarenal mechanisms (overfilling theory).
Sodium accumulation originating from the kidneys is caused by increased sodium absorption in the cortical collecting ducts and collecting ducts as a result of Na -K- ATPase production in the basolateral membrane and increased permeability in the epithelial sodium channels (ENaC) in the apical membrane. In addition, the lack of response to the natriuretic response of atrial natriuretic peptide (ANP) in the medullary collecting ducts is also effective, and it is reported that this is not fully related to aldosterone [30, 31].
4.3.5 Hyperlipidemia and hyperlipoproteinemia
Plasma concentrations of cholesterol, triglycerides, phospholipids, and fatty acids are increased in NS. Generally, there is an inverse relationship between serum albumin level and cholesterol level 3. The level of triglycerides is more variable and may be within normal limits in mild hypoalbuminemia [29, 32].
Like hypoalbuminemia, hyperlipidemia results from increased synthesis or decreased degradation. Increased synthesis is usually associated with increased albumin synthesis [33]. Because lipoproteins and albumin are synthesized in the liver by metabolic pathways that are very close to each other. Decreased lipoprotein catabolism, accompanied by a decrease in lipase activity, also contributes to hyperlipidemia [34].
4.4 Laboratory findings
Laboratory evaluation in patients with (NS); diagnosis and determination of severity of NS are performed to determine possible etiological factors and to make a definitive histological diagnosis with renal biopsy [18].
Urinary stick shows proteinuria and hematuria, and microscopy shows hyaline casts and fat bodies. The presence of erythrocytes, granular, waxy, and wide casts is a finding in favor of glomerulonephritis other than MCD [17, 18].
quantitative proteinuria. In children, normal values are defined as <4 mg/m2/ hr. and the nephrotic border is defined as >40 mg/m2/ hr. While the urine protein/ creatinine ratio is 0.2 in normal, this ratio rises to 2.0 in NS. The serum albumin value of patients with NS is below 2.5 mg/dl. Alpha 2 and beta-globulin levels increased due to increased hepatic synthesis [17, 18]. While the serum IgG level decreases. IgM and IgE levels increase. Serum cholesterol and triglyceride levels increased. Evaluation of BUN and serum creatinine is necessary for kidney functions [17, 18, 22].
Serum complement level, hypertension, and macroscopic should be measured in patients with hematuria or reduced renal function. While complement level is normal in MCD, it is low in APSGN, MPGN, and SLE. Serological evaluation for hepatitis and syphilis should be performed. It is also necessary to conduct research on HIV in patients in the risk group. Secondary for SLE, ANA should be investigated in anti-DNA as it causes NS [18].
For years, scientific institutions and communities dealing with the kidney have debated whether hemodynamic changes alone are responsible for glomerular and tubulointerstitial damage and whether other mechanisms are involved in this process [35].
Recent studies have shown that proteinuria itself, which is a determinant of the severity of some kidney diseases, is harmful. In this context, the amount of protein detected in the urine appears to be the most important factor determining the progression to end-stage renal failure, sometimes to a greater extent than the original disease [36].
Increased proteinuria leads to a progression of renal disease by causing excessive protein uptake by the proximal tubule cells with an inflammatory phenotype and ultimately progressive renal interstitial damage [37]. Proteinuria is associated with the proliferation and apoptosis of proximal tubular cells and interstitial inflammation [38].
5. Conclusion
As a conclusion, starting treatment as early as possible to prevent proteinuria that occurs in cases of nephritis, (NS), and nephrosis will prevent the development of hypoalbuminemia and hyperlipidemia. Proteinuria can be reduced by suppressing the factors that cause increased permeability in the filtration barrier. It is also known that reactive oxygen radicals play a role in (NS), so avoiding oxidative stress may also slow the progression of the disease. Inflammatory kidney diseases such as chronic glomerulonephritis and hereditary polycystic kidney disease are among the kidney diseases that can lead to chronic kidney failure. People at risk for chronic kidney failure; Those who are overweight, have high blood pressure, are diabetic, and have a family history of kidney disease. Lifestyle changes are of great importance in delaying the progression of chronic kidney diseases. Since the kidneys are very rich in blood vessels, all measures that protect our cardiovascular system also have a protective effect on the kidneys.
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