URINARY DYNAMICS IN CHRONIC KIDNEY DISEASES

URINARY DYNAMICS IN CHRONIC KIDNEY DISEASES

Aman Kumar, Akash Yadav * and Dinesh Kumar Jain

Indore Professional Studies Academy, College of Pharmacy, Indore, Madhya Pradesh, India.

ABSTRACT: This review explores the intricate physiology of urine formation and its critical relationship with chronic kidney disease (CKD). Urine formation involves three key processes: glomerular filtration, tubular reabsorption, and tubular secretion, which work together to maintain homeostasis by regulating fluid balance and waste elimination. In CKD, these functions are impaired due to progressive damage to the nephrons, leading to a reduced glomerular filtration rate (GFR) and accumulation of toxic metabolites, which contribute to a variety of complications including hypertension, electrolyte imbalance, and fluid overload. Understanding the mechanisms underlying urine production provides important insights into the pathophysiology of CKD and highlights the importance of early detection and treatment strategies. This review aims to highlight the importance of preserving renal function and improving treatment outcomes in patients with CKD by reviewing current research and clinical practice.

Keywords: Relevant physiology of urine formation, Chronic kidney disease, Future perceptive

INTRODUCTION: The kidneys play a crucial role in maintaining homeostasis by regulating fluid balance, electrolyte levels, and waste elimination through urine formation. This complex process involves three key steps: glomerular filtration, tubular reabsorption, and tubular secretion. These mechanisms work together to ensure the body’s internal environment remains stable, which is essential for overall health and well-being.  Chronic kidney disease (CKD) is a progressive condition marked by the gradual loss of kidney function, often caused by underlying factors such as diabetes and hypertension. Over time, repeated damage to the nephrons diminishes the kidneys' ability to filter blood effectively and produce urine.

This decline in kidney function can result in serious complications, including fluid overload, electrolyte imbalances, and an increased risk of cardiovascular disease. Understanding the physiology of urine formation is vital for comprehending the pathophysiological changes that occur in CKD. Such knowledge provides insight into how impaired kidney function disrupts homeostasis and contributes to the progression of the disease.

Early detection of CKD is critical, as timely interventions can help preserve kidney function and prevent or delay complications. This review focuses on the intricate connection between the processes of urine formation and CKD progression.

It highlights the importance of identifying CKD in its early stages and implementing effective management strategies to improve patient outcomes. By advancing our understanding of these relationships, we can develop better approaches to mitigating the impact of CKD and enhancing the quality of life for affected individuals ^1-5.

Relevant Physiology of Urine Formation: The formation of urine begins with glomerular filtration (GF) in the case of fornication. As a rule, about 180 liters of fluid are filtered every day. All soluble blood components are removed by plasma proteins (and related substances) and lipids are filtered by the beads. More than 99% of the glomerular filtrate is reabsorbed by the renal tubules. Approximately 1.5 liters of urine is produced in 24 hours.

Diuretics act primarily by inhibiting renal tubular reabsorption. A 1% decrease in tubular reabsorption can more than double urine volume. The mechanisms that move ions across tubular cells are complex and involve multiple energy-dependent transmembrane pumps as well as channels between closely adjacent proximal tubule (PT) cells. All Na +falling into the urinary tube cells via the cleaning membrane is pumped up in the intelligence of the kidney on the basement membrane using at Atpase. Since K +has a large cage with an extracellular gradient, the antiport of NA +-K +conditions increase the K +canal. For simplicity, tubular recovery can be divided into four regions ⁶.

Site I: Proximal tubule four mechanisms of Na+ transport have been defined in this segment (a) Direct entry of Na+ via favourable electrochemical gradient. It is an electrogene. (b) Active-coupled Na+ and K+ transport reabsorption of glucose, amino acids, other organic anions and PO4³¯ using special symporters. There is only glucose-coupled Na+ reabsorption electrogene. (c) Exchange with H+: Pt -Ties releases H+ from Na+-H+ anti -porters (Exchange Na+-h+) in the light film. This replacement moves Na+ from urinary tipon to internal cells. The released H+ combines with HCO3. Carbon dioxide is formed in the tubular fluid. This H2CO3 is split into H2O + CO2 attached to the brush border, as it is very slowly decomposed in part by H2CO3 (type IV enzyme). Practically all HCO3 ¯ is reabsorbed in PT by this mechanism, because tubular membrane, as such, is relatively impermeable to HCO3-. (d) Disproportionately large reabsorption of HCO3 ¯ acetate, PO4 3¯, amino acids, and other anions creates passive driving forces for Cl¯ diffusion through the paracellular pathway (between tubular cells), especially in late PT. This takes up Na+ and water to maintain electrical neutrality and isotonicity; reabsorption in the PT is isotonic. A major part of filtered K+ is reabsorbed in the PT. Thus, an isotonic tubular fluid with major changes in composition enters the thin descending limb of loop of Henle.

Section II: Ascending Loop of Henle (Asc LH). The thick part of the Asc LH can be divided into two distinct parts: (i) the medulla, lined with cuboidal cells. (ii) the cortex, lined with flattened cells. Both parts are relatively impermeable to water but actively absorb salt, diluting the tubular fluid. In the brain, another luminal membrane transporter transports ions in the stoichiometric ratio Na+-K+-2Clâ and is not electrogenic. Na+ that enters the cell is pumped into the e.c.f. Na+ K+ ATPase on the basolateral membrane. In addition, the Na+-Cl¯ symporter moves Cl¯ down its electrochemical gradient into the e.c.f. and transports Na+. As the tubular fluid passes through the AscLH, it becomes progressively hypotonic. Accumulation of NaCl in the medullary interstitium without water makes the medullary interstitium hypertonic and establishes a corticomedullary osmotic gradient: it draws water from the descending limb of the loop of Henle (this thin segment is highly permeable to water but has no active transport of NaCl), so that the fluid entering the AscLH becomes hypertonic.

Site III: Diluting cortical segment of the loop of Henle this segment, also impermeable to water, continues to absorb salt, but here it is via a Na+-Cl¯ symporter. The luminal fluid becomes further diluted. Site III: Cortical diluting segment of loop of Henle this segment, also impermeable to water, continues to absorb salt, but here it is through a Na+-Cl¯ symporter. Tubular fluid gets further diluted.

Site IV: Distal tubule (DT) and collecting duct (CD) in the late DT and late CD, Na+ is again actively reabsorbed. Cation and anion balance is maintained partly by passive diffusion of Cl- and partly by secretion of K+ and H+. Na+ uptake at this site occurs via specific amiloride-sensitive Na+ channels and is largely controlled by aldosterone (see diagram). This allows you to precisely regulate your electrolyte production according to your body's needs. Like other cells, DT and CD cells are rich in K+; there is a chemical gradient for its diffusion into the tubule lumen, facilitated by the negative transepithelial potential difference of the lumen in this part of the tubule. The luminal membrane has an active secretory pump for H+ which is in turn regulated by the movement of Na+ in the opposite direction. Diuretics acting near aldosterone-sensitive ion exchange sites increase the supply of Na + to the distal nephron and increase its exchange for K+, which is therefore reabsorbed into the PT and AscLH and secreted into the DT and CD. The net loss of K+ is regulated by changes in secretory processes and depends on:

1. The Na+ load delivered to distal segment
2. Presence or absence of aldosterone
3. (Availability of H+
4. Intracellular K+ stores

Free Water Clearance: Free water clearance refers to the amount of urine excreted per unit time that exceeds the volume needed to excrete solutes in isotonic equilibrium with plasma. This value is positive when dilute urine is produced in the absence of antidiuretic hormone (ADH) and negative when concentrated urine is formed under the influence of ADH. When urine is isotonic, free water clearance is zero, regardless of the urine volume. The generation of both positive and negative free water clearance relies on the establishment of a cortico-medullary osmotic gradient, a process inhibited by diuretics acting on the medullary ascending limb of the loop of Henle (AscLH).  In the proximal tubule (PT), organic ion transport operates through a nonspecific bidirectional active transport system for organic acids and bases. However, the extent of transport varies between substances. For instance, uric acid is typically reabsorbed to a greater extent than it is secreted, while the opposite is true for penicillin.

Several clinically significant diuretics, including furosemide, thiazides, and amiloride, utilize this transport mechanism to reach their sites of action on the luminal side of the renal tubule, particularly in the AscLH, distal tubule (DT), and collecting duct (CD). These diuretics target specific processes to influence urine composition and volume, playing a vital role in the treatment of various renal and cardiovascular conditions.

Chronic Kidney Drug: Chronic kidney disease (CKD) is a prevalent health condition, affecting an estimated 800 million individuals globally. According to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines, the measurement or estimation of glomerular filtration rate (GFR) is a cornerstone in the diagnosis and management of CKD. GFR assessment provides critical insights into the severity and progression of the disease, enabling clinicians to implement timely interventions.

Early detection and effective management of CKD are essential to prevent its progression and reduce the risk of complications, including cardiovascular diseases and kidney failure.  GFR measurement or estimation is widely regarded as an invaluable diagnostic tool for CKD. It helps determine the functional status of the kidneys and guides treatment decisions. In addition to GFR, biochemical markers and urinary biomarkers play a significant role in understanding CKD pathogenesis and progression. Albuminuria, a key biomarker, is both accessible and cost-effective, often detected through standardized urinalysis test strips. It serves as an early indicator of CKD and is strongly associated with an increased risk of cardiovascular events. The level of proteinuria is directly proportional to cardiovascular risk, emphasizing the importance of regular monitoring in CKD patients.  Chronic kidney damage can be diagnosed when abnormal kidney function persists for at least three months or when albuminuria is detected despite normal kidney function. Structural or morphological abnormalities, such as polycystic kidney disease in adults, also indicate CKD. During the disease’s progression, irreversible damage to the glomeruli and tubules often occurs, which can be anticipated using advanced biochemical markers.

Amiloride, a diuretic, utilizes the transport mechanism in the proximal tubule to reach its site of action on the luminal side of the renal tubule, particularly in the ascending limb of the loop of Henle (AscLH), distal tubule (DT), and collecting duct (CD). This mechanism underscores the intricate interplay of transport systems in the kidneys and their relevance in both disease pathogenesis and treatment strategies. A comprehensive understanding of these processes is vital for developing effective diagnostic and therapeutic approaches in CKD management ^7-12.

Chronic Medications for Renal Therapy: The Kidney Disease Improving Global Outcomes (KDIGO) guidelines recommend that measurement or estimation of glomerular filtration rate (GFR) is an important diagnostic tool for CKD ¹³. Early diagnosis and treatment of CKD are essential to prevent disease progression and minimize the risk of side effects. Accurate assessment of SCF is important in this regard as it provides valuable information on the severity and progression of CKD. Measurement or assessment of SCF is widely recognized as important in the diagnosis and treatment of CKD and is important in clinical guidelines ¹⁴. 

A five-stage classification system based on GFR levels provides clinicians with a basis to assess the severity of CKD and adapt treatment strategies accordingly Table 1 many diseases and potentially toxic substances are involved in the development of CKD. However, during the pathogenesis of CKD, irreversible damage to the glomeruli and tubules develops, which can be predicted using several biochemical markers ¹⁵. In the early stages of CKD, albuminuria is the most readily available and standardized urinary biomarker, and the use of urine dipstick tests is cost-effective. Albuminuria is a predictor of CKD and further increases the risk of cardiovascular disease ^{14, 16}.

Cardiovascular risk also depends on the level of proteinuria. Chronic kidney disease may be diagnosed if renal failure persists for at least 3 months or if abnormal albuminuria is detected despite normal renal function. CKD can also manifest as structural or morphological abnormalities of the kidney (e.g., polycystic kidney disease in adults) ¹³. The gradual decrease in the number of nephrons has been identified as a significant factor in the gradual narrowing of the glomerular filtration rate (GFR). As CKD progresses, the renal function gradually declines. Typical uremic symptoms are observed in patients with severely advanced and untreated kidney damage. Along with the gradual deterioration of kidney function, many accompanying clinical symptoms can be observed as a result of impaired physiological function of the kidneys.

TABLE 1: STAGES OF CHRONIC KIDNEY DISEASE (CKD) BASED ON ESTIMATED GLOMERULAR FILTRATION RATE (EGFR)

Slowing the Progression of Chronic Kidney disease: Kidney support contains two important tasks. Prevention and deceleration of chronic kidney disease (CBP) and its progress. HBP people have a significant risk of incidence and mortality due to cardiovascular disease, regardless of whether they are suffering from diabetes and high blood pressure. Moreover, the risk of death from chronic kidney disease, especially cardiovascular disease, is higher than the risk of death required to initiate renal replacement therapy ^{17, 18}. Therefore, it is crucial to prevent kidney disease and the progression of CKD. Addressing the underlying conditions that cause CKD is essential to slowing its progression. For instance, treatment of Autosomal Polycystic Kidney Disease (ADPKD), diabetes, hypertension, primary glomerular diseases, and hematological diseases is recommended. The simplest approach to slowing the progression of kidney disease is to rapidly manage reversible processes, such as possible obstruction of urine flow.

Clinical studies have demonstrated that a protein intake of 0.8 g/kg body weight/day reduces the progression of CKD ²⁰. Adopting a low-salt diet will not only help regulate your blood pressure but also reduce salt retention. It is recommended that your daily sodium intake from food not exceed 2-3g, or about 5g of table salt. By following these tips, you can significantly reduce your risk of developing hypertension and related cardiovascular diseases ^20-21. Reducing salt intake does not imply the use of sodium bicarbonate therapy to treat metabolic acidosis.

Several published studies have confirmed that administration of sodium bicarbonate has no significant effect on systemic blood pressure ^{23, 24}.

Angiotensin-converting Enzyme Inhibitors: The benefits of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) in reducing the risk of cardiovascular events (CVEs) and delaying end-stage renal disease (ESRD) in patients with CKD are well established [39–41]. In the absence of contraindications, clinicians may choose to use ACEIs to treat hypertension, while ARBs are used in cases of intolerance ²⁷. Resistant hypertension is common in CKD and multiple antihypertensive treatments may be required ²⁸.

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) have been acknowledged for their role in reducing urinary protein excretion, preserving kidney function, and slowing the progression of chronic kidney disease (CKD). These drugs decrease intraglomerular pressure and reduce the production of primary ultrafiltrate, thereby lessening the reabsorption load on the tubular epithelium. This reduces the volume of fluids, electrolytes, and organic substances that must be processed by the tubules. While ACEIs do not directly alter renal blood flow, they are known to relatively improve cerebral blood flow.  The renal benefits of ACEIs and ARBs are most prominent in CKD patients with proteinuria, as summarized in Fig. 1. However, in certain cases, their use can lead to worsening renal function and elevated serum potassium levels, necessitating discontinuation as antihypertensives. In severe kidney injury, it is critical to assess the continued use of these drugs. Interestingly, discontinuing ACEIs or ARBs in advanced CKD does not usually improve renal function significantly. On the contrary, it may heighten the risk of extracellular volume (ECV) expansion and accelerate the progression to renal failure. Therefore, ACEIs and ARBs remain key in managing CKD but require careful monitoring and tailored use in patients with advanced renal impairment ^29-32.

FIG. 1: THE ALREADY “CLASSIC” ACEI/ARB DRUG EXERT THEIR RENAL PROTECTIVE EFFECT BY REDUCING INTRAGLOMERULAR PRESSURE. Abbreviation: Ace-1: Angiotensin Convertase Enzyme Inhibitors.

Avoiding Nonsteroidal Anti-inflammatory Drugs: Non-steroidal anti-inflammatory drugs (NSAIDs) impact kidney function by inhibiting the production of prostaglandins, which are essential for maintaining renal blood flow. This occurs through the inhibition of cyclooxygenase enzymes (COX-1 and COX-2), leading to vasoconstriction in renal blood vessels and reduced glomerular blood circulation. Additionally, NSAIDs can contribute to salt retention, which may result in elevated blood pressure and increased strain on the kidneys. Long-term use of NSAIDs poses significant risks, particularly in older adults, as it can lead to irreversible kidney damage over time. These effects underscore the importance of using NSAIDs cautiously.

They should primarily be reserved for managing acute medical conditions rather than for chronic use, except in cases where their benefits outweigh the risks. Proper monitoring and alternative therapies are recommended to minimize potential harm to kidney function, especially in vulnerable populations.

Use of Sodium-glucose Cotransporter-2 (SGLT2) Inhibitors: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are essential therapeutic agents widely used in the management of kidney disease and chronic kidney disease (CKD). Approved by the U.S. Food and Drug Administration (FDA) in 2013, these drugs were initially introduced for the treatment of type 2 diabetes due to their ability to effectively reduce blood sugar levels.

They achieve this by inhibiting glucose reabsorption in the proximal tubules of the kidneys, leading to increased glucose excretion through urine, which helps manage hyperglycemia Fig. 2. Beyond their role in diabetes management, SGLT2 inhibitors have proven beneficial in treating heart failure, showcasing their versatility and importance in managing multiple chronic conditions. These drugs not only lower blood sugar but also provide significant renal and cardiovascular protection. As a result, they have become a cornerstone in therapeutic strategies, offering a comprehensive approach to improving outcomes for patients with type 2 diabetes, CKD, and heart failure.

FIG. 2: THE THERAPEUTIC EFFECT OF SGLT2 INHIBITORS IS THE INCREASED EXCRETION OF GLUCOSE AND SODIUM, WHICH BY STANDING OTHER PHYSIOLOGICAL PROCESSES, WE CAN EXPERIENCE THE BENEFICIAL EFFECT OF SUCH TREATMENT, FOR EXAMPLE, IN HEART FAILURE OR IN SLOWING DOWN THE PROGRESSION OF CKD. Abbreviation: ATPase: Adenosine 5-TriPhosphatase, Na, natrium, K, potassium, Glut2: glucose transporter 2, SGLT2, sodium/glucose cotransporter 2.

Additionally, SGLT2 inhibitors reduce sodium reabsorption, which leads to increased natriuresis and effectively represents a mild add-on diuretic effect ³³. Nevertheless, the entry of sodium into the macula densa was augmented, normalizing the tubuloglomerular feedback. The resulting afferent arteriolar vasoconstriction leads to a decrease in intraglomerular pressure ^34-35.

SGLT2 inhibitors have been shown to slow CKD progression even in non-diabetic and proteinuria patients ^{13, 19, 36, 37}. Based on 1B evidence, guidelines recommend the use of SGLT2 inhibitors in CKD patients with appropriate RAAS inhibition ¹³.

Mineralocorticoid Receptor Blockade (MRA): Aldosterone is a steroid hormone that plays a key role in regulating the activity of mineralocorticoids. It is synthesized in the zona glomerulosa of the adrenal cortex and primarily functions to promote sodium reabsorption and potassium excretion within the cortical collecting duct of the renal system. This mechanism is essential for maintaining fluid and electrolyte balance, blood pressure regulation, and overall homeostasis. However, recent research has highlighted aldosterone’s significant role in the development of cardiovascular and renal diseases, with its overactivation contributing to severe pathological changes.  In the cardiovascular system, aldosterone exerts various detrimental effects. It promotes myocardial hypertrophy, ventricular remodeling, and meningeal inflammation, which can exacerbate heart failure. Additionally, aldosterone reduces coronary blood flow and contributes to myocardial ischemia, further aggravating cardiovascular disease progression.

These harmful effects underscore the importance of managing aldosterone activity in patients with cardiovascular conditions. Similarly, aldosterone adversely affects the renal system. It is associated with glomerular hypertrophy, glomerulosclerosis, proteinuria, and progressive kidney damage. Proteinuria, in particular, is a critical marker of kidney damage and disease progression in chronic kidney disease (CKD). The cumulative effects of aldosterone on the cardiovascular and renal systems make it a crucial target in managing these diseases. To slow CKD progression, aldosterone antagonists are frequently used in combination with ACE inhibitors or angiotensin receptor blockers (ARBs). This combination therapy has proven effective in reducing proteinuria, thereby protecting kidney function. However, the use of aldosterone antagonists carries the risk of hyperkalemia, a condition marked by elevated potassium levels in the blood.

Hyperkalemia is particularly concerning for patients with CKD or those receiving ACE inhibitors/ARBs, as it can exacerbate cardiovascular and renal complications.  Patients who experience mild hyperkalemia during ACE inhibitor or ARB therapy may also develop non-anion gap metabolic acidosis (NAGMA), a mild form of metabolic acidosis. In such cases, sodium bicarbonate (NaHCO3) supplementation is often recommended. This approach not only helps correct metabolic acidosis but also improves and potentially reverses hyperkalemia, restoring electrolyte balance.  While aldosterone antagonists are effective, nonsteroidal mineralocorticoid receptor antagonists (MRAs) have emerged as a safer and more selective alternative. These agents provide significant reductions in proteinuria with a much lower risk of causing hyperkalemia. One such nonsteroidal MRA is finerenone, which has demonstrated promising results in clinical studies. Finerenone effectively reduces albuminuria, a marker of kidney damage, and levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), a biomarker associated with heart failure.

Importantly, finerenone achieves these benefits without increasing the risk of hyperkalemia, making it a safer option for patients with CKD and cardiovascular conditions. The harmful effects of aldosterone on both the cardiovascular and renal systems highlight the need for effective therapeutic strategies.

With advancements in treatment options, such as the introduction of nonsteroidal MRAs like finerenone, clinicians can better manage the risks associated with aldosterone overactivation. By addressing proteinuria and minimizing adverse side effects, these therapies offer a promising path toward improving patient outcomes in CKD and cardiovascular disease management ^39-41.

FIG. 3: THE AMELIORATION OF ALDOSTERONE ACTIVITY BY REDUCING OR INHIBITING ITS FUNCTION IS HIGHLY BENEFICIAL TO THE CARDIOVASCULAR SYSTEM. IN ADDITION, IT IS AN EFFECTIVE MEASURE FOR SLOWING THE PROGRESSION OF CHRONIC KIDNEY DISEASE (CKD). Abbreviations: AP-1: Activator protein 1; MRA, mineralocorticoid receptor antagonist; NO, nitrogen monoxide; NADPH, nicotinamide adenine dinucleotide phosphate oxidase; NF-B: Nuclear factor kappa-light-chain-enhancer of activated B cells; ROS: Reactive oxygen species; SGK-1: Serine/threonine-protein kinase

Treatment of Renal Anaemia: Renal anemia can occur in the early stages of CKD (stage 3a). Anemia leads to tissue hypoxia, contributing to further progression ⁴². It is plausible that ameliorating anemia would improve oxygen delivery to the medulla. Renal anemia is caused by reduced erythropoietin production ⁴³. A diagnosis can be made if other causes, such as iron deficiency, are ruled out ^{44, 45}. If the patient’s hemoglobin concentration is consistently below 11 g/dl (HTC < 0.33 %).and secondary causes of anemia can be ruled out, erythropoietin treatment should be initiated (13). In contemporary medical practice, a wide range of medications are available to stimulate the production of red blood cells ⁴⁶. Human recombinant erythropoietin products are among these drugs. Hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) agents are currently available for this purpose.

CKD-metabolic Bone disease: Retention begins in the early stages of CKD and contributes to the development of secondary hyperparathyroidism. Properly regulating mineral and bone metabolism relies on the function of various hormones that oversee the calcium and phosphate levels. These hormones consist of parathyroid hormone (PTH), calcidiol or 25 (OH)D3 (which is the precursor of calcitriol), calcitriol or,25 (Hyperphosphatemia is a common complication of chronic kidney disease (CKD). Phosphate OH)2D3 (the most potent form of the vitamin D hormone system), calcitonin, and FGF23/klotho.

These hormones play a significant role in maintaining bone health and metabolism. CKD can significantly alter various body parameters, including calcium, phosphate, PTH, FGF23/Klotho, and the vitamin D hormonal system, encompassing calcidiol and calcitriol. These changes can affect bone and vascular metabolism, ultimately leading to adverse clinical outcomes such as decreased bone mass, increased fragility fractures, and vascular and valvular calcification ⁴⁷.

CONCLUSIONS: Urine formation is a critical physiological process involving glomerular filtration, tubular reabsorption, and tubular secretion, all of which maintain fluid and electrolyte balance and eliminate metabolic waste. Chronic kidney disease (CKD) disrupts these processes due to progressive nephron damage, leading to a decreased glomerular filtration rate (GFR) and subsequent accumulation of toxic metabolites. This disorder leads to various complications, including hypertension, electrolyte imbalance, and fluid overload, which significantly affect the patient's quality of life.

Understanding the basic physiology of urine production provides significant insights into the mechanisms of CKD and highlights the importance of early detection and treatment strategies. Interventions such as lifestyle modifications, drug therapy, and monitoring of kidney function are essential to slow disease progression. Ultimately, this knowledge highlights the need for continued research and clinical vigilance to improve outcomes for patients with CKD and highlights the complex relationship between kidney function and overall heal.

ACKNOWLEDGEMENT: I would like to express my sincere gratitude to all those who have supported and contributed to the completion of this article. I would like to convey my heartfelt thanks and respect towards IPS Academy College of Pharmacy, Indore for providing me with the necessary and helping me throughout my work. Lastly, I would like to thank my family and friends for their continuous encouragement and understanding, which provided the motivation to complete this article.

CONFLICTS OF INTEREST: The authors have no conflicts of interest.

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    How to cite this article:

    Kumar A, Yadav A and Jain DK: Urinary dynamics in chronic kidney diseases. Int J Pharm Sci & Res 2025; 16(5): 1159-68. doi: 10.13040/IJPSR.0975-8232.16(5).1159-68.

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