Lessons learned from the Japanese nephritis screening study

A program of urine screening for asymptomatic hematuria and proteinuria in school children has been conducted since 1973 by the Ministry of Education in Japan with great success in the early detection of asymptomatic renal disease. In order to know whether this nationwide program during 13 years has contributed to understanding of the epidemiology of chronic glomerular disease in Japan, a multicenter survey of the patients was conducted. Between 70% and 80% of IgA and non-IgA mesangial proliferative glomerulonephritis and 65%–80% of membranoproliferative glomerulonephritis (MPGN) were detected by mass urine screening at school. Severe glomerular lesions were more frequently observed in children with chance proteinuria and hematuria, as well as IgA and non-IgA mesangial proliferative glomerulonephritis with significant proteinuria. Mild glomerular change was more frequent in patients with MPGN, IgA and non-IgA mesangial proliferative nephritis with minimal proteinuria who were detected by our screening program, rather than those seen with some of the nephritic signs and symptoms at diagnosis. The above evidence suggests that a screening program may open the way for the early management of these diseases, especially where treatment is alrealy established.     

肾活检患者451例临床与病理构成对比分析

目的 分析珠海地区肾脏疾病的病理及临床特点.方法 回顾性分析我院451例肾活检患者的临床及病理资料,探讨其病因、临床特点及病理类型的关系.结果 451例肾活检患者中,男、女高峰发病年龄为19～37岁,分别占59%及65%.原发性肾小球疾病共369例（占81.81%）,临床类型排在前3位的依次为无症状血尿、蛋白尿149例（占40.38%）、慢性肾小球肾炎104例（占28.18%）、肾病综合征76例（占20.60%）,病理类型排在前3位的依次为IgA肾病251例（占68.02%）、系膜增生性肾小球肾炎（MsPGN）33例（占8.94%）、微小病变型肾病（MCD）24例（占6.50%）;继发性肾小球疾病69例（占15.30%）,临床类型排在前3位的依次为狼疮肾炎26例（占37.68%）、乙型肝炎相关性肾小球肾炎24例（占34.78%）、紫癜肾炎9例（占13.04%）.结论 原发性肾小球疾病是目前最主要的肾小球疾病,IgA肾病在原发性肾脏疾病中发病率最高,继发性肾小球疾病中狼疮肾炎排在首位.     

Assessment of the effect of mesangial hypercellularity in childhood nephropathies to the clinical and laboratory findings

Aim: To assess the relationship between mesangial hypercellularity in various childhood nephropathies and clinical and laboratory parameters. Methods and patients: The reports of the renal biopsies were evaluated retrospectively. The patients with diagnosis of IgA nephropathy (isolated and Henoch–Schönlein nephritis), IgM nephropathy, or isolated mesangial proliferative glomerulonephritis were included. Each nephropathy group was divided into two subgroups according to the severity of mesangial hypercellularity as mild and severe. The biochemical data and histopathological findings of the patients were recorded. Results: When the groups were compared, it was found that the patients with IgA nephropathy had hematuria (p?=?0.043) and the patients with IgM nephropathy had nephrotic syndrome more frequently than the other patients (p?=?0.01). No difference was detected between the groups regarding the severity of mesangial hypercellularity. On the other hand, when the groups were evaluated within themselves, no significant association was detected between the severity of mesangial hypercellularity and clinical and laboratory parameters. It was determined that the renal biopsy was performed earlier in patients with Henoch–Schönlein nephritis compared to the other cases (p?=?0.004). Compared to the isolated IgA nephropathy group, it was found that the number of cases with severe mesangial hypercellularity was higher and the level of proteinuria was more prominent in patients with Henoch–Schönlein nephritis. Additionally, when the patients with Henoch–Schönlein nephritis were evaluated, the degree of proteinuria was found to be higher in patients with severe mesangial hypercellularity compared to those of showing mild mesangial hypercellularity (p?=?0.002). Conclusion: It was observed that there is no direct relation between the severity of mesangial hypercellularity and clinical and laboratory findings in various childhood nephropathies. However, when Henoch–Schönlein nephritis is compared with IgA nephropathy, it was found that the severity of mesangial hypercellularity was higher in cases with Henoch–Schönlein nephritis and the level of proteinuria was more prominent in those cases. However, no difference was detected in glomerular filtration rates and biochemical data with regard to the level of mesangial hypercellularity.     

IgA-associated glomerulonephritis with membranoproliferative glomerulonephritis-like pattern in two children

In this article, we report two patients with IgA-associated glomerulonephritis with a membranoproliferative glomerulonephritis (MPGN) -like pattern. Both patients had nephrotic syndrome at onset. One patient was treated with high-dose alternate-day prednisolone (PSL), and the other with indomethacin and low-dose PSL. One lost the urinary abnormalities 3 years after starting treatment. The other lost the nephrotic state and hematuria over a 5-year period, but proteinuria persisted until the last follow-up. Both patients had diffuse proliferative changes with mesangial interposition and subendothelial deposits, associated with strongly positive deposits of C3 and IgA along the capillary walls of the glomeruli. These two patients showed histological changes compatible with type-I MPGN, but the pattern of IgA deposits was not typical of idiopathic MPGN or IgA nephropathy. We assume this is a rare form of MPGN, not associated with liver disease or other systemic diseases.     

Acute poststreptococcal glomerulonephritis superimposed on IgA nephropathy

Superimposition of poststreptococcal glomerulonephritis (PSGN) on the course of IgA nephropathy (IgAN) is uncommon. A case of PSGN during IgA nephropathy is presented. A 30-year-old man who had alternating gross and microscopic hematuria for 7 months underwent a renal biopsy. The first renal biopsy revealed IgAN with mesangial deposits of IgA and C3. Two months later, the patient suffered generalized edema, proteinuria, hematuria, an increased ASO titer and a decreased C3 level. A second renal biopsy revealed diffuse endocapillary proliferative glomerulonephritis with epimembranous hump-like electron-dense deposits of C3, but the original mesangial IgA deposits had disappeared. A diagnosis of acute PSGN was indicated. Two months after the onset of acute nephritic syndrome, the patient remained asymptomatic, except for microscopic hematuria and proteinuria. Some cases with persistent proteinuria or hematuria after PSGN are probably related to preexisting IgAN.     

原发性肾病综合征并发急性肾损伤48例临床病理分析

目的探讨原发性肾病综合征合并急性肾损伤的临床及病理特点,提高此类并发症的防治水平。方法对我院原发性肾病综合征合并急性肾损伤患者的临床和病理改变进行回顾性分析。结果原发性肾病综合征合并急性肾损伤的临床特征表现为大量蛋白尿、高度水肿,常合并胸腹腔积液。肾脏病理类型：系膜增生性肾小球肾炎、肾小球微小病变及IgA肾病多见。其中系膜增生性肾小球肾炎22例,占46%;微小病变型10例,IgA肾病9例。所有患者均依据病理分型给予激素和（或）细胞毒药物,同时行利尿、控制感染、抗凝等综合治疗,其中5例进行血液透析治疗,肾损伤大多好转,但增生硬化型肾炎等预后较差。结论原发性肾病综合征并发急性肾损伤临床并不少见,多发生于系膜增生性肾小球肾炎、肾小球微小病变及IgA肾病,尽早明确病理诊断和去除诱因,并予相应治疗,大多患者预后良好,肾功能可恢复正常。     

Extrarenal cytokines modulate the glomerular response to IgA immune complexes.

Clinical episodes of IgA nephropathy coincide recurrently with microbial infections. Cytokines produced during such infections may play a role in the pathogenesis of IgA-associated glomerulonephritis. To test this hypothesis, we examined the influence of passively administered proinflammatory cytokines (IL-1, IFN-gamma and IL-6) on the development of glomerulonephritis in an experimental model of IgA nephropathy. Glomerular IgA immune deposits were induced in mice by administration of IgA anti-phosphorylcholine (PC) with either a PC-containing carbohydrate antigen of Pneumococcal C polysaccharide (PnC) or a protein antigen of PC-conjugated bovine serum albumin (PC-BSA). The effect of IL-1 on the IgA-PC-BSA induced glomerular changes resulted in an increase of mesangial hypercellularity that was associated with mild proteinuria and hematuria. Mice treated with IL-1 and IgA-PnC developed diffuse proliferative glomerulonephritis with proteinuria and hematuria. In contrast, IL-6 treatment with IgA-PC-BSA of IgA-PnC failed to exert any significant renal effect. The combination of IL-6 and IL-1, however, intensified the mesangial hypercellularity of the IgA-PC-BSA, and induced severe proliferative glomerulonephritis with inflammatory monocytes and neutrophils infiltrates in the IgA-PnC treated mice. These glomerular changes were also accompanied by increased proteinuria and hematuria. Similarly, the combination of IFN with IL-1 produced histologic changes and compromised renal function more than IFN or IL-1 exerted independently. These results suggest that extrarenal cytokines influence the renal response to IgA immune deposits. We also conclude that a synergy of multiple cytokines and nephritogenic antigens immobilized in glomerular IgA immune deposits may lead to rapid progression of IgA-associated glomerulonephritis.     

IgA nephritis in Beh?et's disease: case report and review of the literature

We describe a 13-year-old girl with the incomplete type of Beh?et's disease who had recurrent oral and genital ulcers, folliculitis, proteinuria and hematuria. Renal biopsy specimens revealed diffuse proliferative glomerulonephritis with strongly positive IgA deposits in the glomerular mesangial area, which is histologically indistinguishable from primary IgA nephritis. Further studies of the IgA subclasses showed that IgA1 deposits were predominant in the glomerular mesangium. Primary IgA nephritis is thought to be associated with polymeric IgA1. So it appears that there may be a common underlying disease or mechanism involved in both primary IgA nephritis and the IgA nephritis in Beh?et's disease.     

Monocyte infiltration and cross-linked fibrin deposition in IgA nephritis and Henoch-Schoenlein purpura nephritis

To clarify the role of immune cell infiltration and fibrin deposition in glomerular injury, renal biopsy specimens taken from patients with primary IgA nephritis and Henoch-Sch?nlein purpura nephritis (HSPN) were evaluated using monoclonal antibodies specific to mononuclear cell surfaces and cross-linked fibrin (XFb). Monocytes/macrophages were the predominant cell type infiltrating glomeruli in IgA nephritis and HSPN. The intraglomerular monocyte population in both diseases was significantly higher than that in normals, mesangial proliferative (non-IgA) glomerulonephritis or minimal change nephrotic syndrome. In IgA nephritis, there was a clear correlation between glomerular monocyte accumulation and the degree of proteinuria. Although the monocyte influx tended to decline with time in HSPN, it remained unchanged in IgA nephritis. XFb deposition was found in the glomeruli of 27 out of 48 patients with IgA nephritis, and in 15 out of 20 with HSPN. The degree of XFb deposition in IgA nephritis correlated significantly with the degree of mesangial proliferation. These findings indicate a close relationship of monocyte/macrophage infiltration and XFb deposition with glomerular injury in IgA nephritis.     

儿童隐匿性肾炎的临床和病理研究

目的：探讨儿童隐匿性肾炎的临床和肾组织病理改变特点及其关系。方法：回顾性分析肾活检的323例隐匿性肾炎患儿的临床和肾组织病理改变情况。结果：323例隐匿性肾炎患儿中，单纯性血尿229例，单纯性蛋白尿19例，血尿伴蛋白尿75例。肾组织病理改变类型包括：轻微病变103例（31，89％）、基本正常74例（22．91％）、IgA肾病（IgAN）73例（22．60％）、薄基底膜病（TBMN）27例（8．36％）、系膜增生性肾炎（MsPGN）18例（5．57％）、局灶增生性肾炎（FPGN）10例（3．10％）、膜性肾病（MN）8例（2，48％）、局灶节段肾小球硬化（舢）8例（2．48％）、微小病变（MCD）1例（0，31％）、IgM肾病（IgMN）1例（0．31％）。单纯性血尿组中肾组织结构基本正常的比例较血尿伴蛋白尿组明显偏高（P〈0，01）；血尿伴蛋白尿组中IgAN的比例高于单纯性血尿组和单纯性蛋白尿组（分别P〈0．01、P〈0．05）。IgAN的Lee分级：单纯性血尿组中Ⅰ、Ⅱ级85．00％，Ⅲ级及以上15．00％；血尿伴蛋白尿组中Ⅰ、Ⅱ级58．10％，Ⅲ级及以上41．90％，明显高于单纯性血尿组（x^2=6．47，P〈0．05）。结论：儿童隐匿性肾炎的病理以轻微病变、基本正常、IgAN为常见表现，血尿伴蛋白尿患儿病变较单纯性血尿患儿为重。     

IgA nephropathy: lessons from an animal model, the ddY mouse

IgA nephropathy is the most common primary chronic glomerulonephritis, and was first described by J. Berger (Transplant Proc. 1969;1:939-944). Histopathologically, IgA nephropathy is characterized by expansion of glomerular mesangial matrix, with mesangial cell proliferation. Glomeruli typically contain generalized-diffuse granular mesangial deposits of IgA, IgG and C3. Since pathogenesis of IgA nephropathy is still obscure, it is important to try to determine the initiation and progression of this disease using a suitable animal model. Several investigators, including Rifai's group (Rhode Island, USA) and Emancipator's group (Cleveland, Ohio, USA), reported various experimental animal models for this disease. In 1985, Imai et al first reported that the ddY strain of mouse can serve as a spontaneous animal model for IgA nephropathy. These mice show mild proteinuria without hematuria, and mesangioproliferative glomerulonephritis with severe glomerular IgA deposits in association with an increase of serum IgA level (Imai et al. Kidney Int. 1985;27:756-761). Electron-dense deposits are observed in the glomerular mesangial areas by electron microscopy. Furthermore, Muso's group succeeded in generating a mouse model of IgA nephropathy with a high incidence and early onset of glomerular IgA deposition (Miyawaki et al. Nephron. 1997;76:201-207). The selection procedure was successful in increasing the serum IgA level of the selected line. The selected ddY line (HIGA mice) showed only mild proteinuria (100-300 mg/dL) and did not show hematuria. These immunohistopathological findings in ddY mice resemble those in IgA nephropathy patients. The objectives of this review are to introduce the genetic background, Th1/Th2 polarization, expansion of extracellular matrices (ECMs) and treatment of IgA nephropathy of the ddY mouse. These findings from the ddY mouse appear to be useful in determining the pathogenesis and treatment of patients with IgA nephropathy.     

IgA肾病520例临床病理分析

目的研究IgA肾病(IgAN)的临床和病理特点及其相互关系。方法对1992年11月～2003年6月温州医学院附属第一医院肾内科病理室肾活检诊断的原发性IgAN520例进行临床与病理分型关系的分析。结果520例IgAN临床表现以无症状性尿检异常最常见,占346例(66.5%),其次是慢性肾炎和肾病综合征,分别占77例(14.8%)和66例(12.7%)。病理类型以局灶节段硬化性肾小球肾炎最常见,占186例(35.8%),其次是系膜增生性肾小球肾炎、轻微病变肾小球肾炎和局灶节段增生性肾小球肾炎,分别为116例(22.3%)、104例(20%)和63例(12.1%)。结论IgAN的临床病理表现多样化并具有一定特点。临床表现最常见为无症状性尿检异常,在病理上最常见的是局灶性肾小球病变类型。     

Studies on circulating immune complexes. II: Circulating immune complexes in primary IgA nephropathy and membranoproliferative glomerulonephritis

A study of circulating immune complexes (CIC) was undertaken in 25 patients with primary IgA nephropathy and 13 patients with membranoproliferative glomerulonephritis (MPGN). Clinically, the 25 patients with IgA nephropathy were divided into two groups: the latent type, characterized by chance proteinuria and/or hematuria; and the acute onset type, revealing acute nephritic syndrome. Both the IgG class of CIC (IgG-IC) and the IgA class of CIC (IgA-IC) were measured by conglutinin binding enzyme immunoassay (C-assay). IgG-IC were found to be positive in 32% of the patients with IgA nephropathy, and in 77% of those with MPGN. IgA-IC were positive in 72% of the patients with IgA nephropathy, and in 54% of those with MPGN. Concerning the acute onset type of IgA nephropathy, IgG-IC and IgA-IC were found in 71% and 86% of the patients, respectively, which was more frequent than in the latent type group. Simultaneous presence of IgA-IC and glomerular IgA deposits detected by an immunofluorescence study was noted in 75% of the patients with IgA nephropathy. On the other hand, 78% of the patients with MPGN revealed IgG-IC and glomerular IgG deposits simultaneously. Thus, IgG-IC and IgA-IC appear to play important roles in the pathogenesis of MPGN and IgA nephropathy, respectively.     

Histology and immunohistology of IgA nephropathy

IgA nephropathy is a histologically diverse glomerular disease characterized by mesangial or mesangial plus peripheral glomerular capillary immune complex deposits that contain IgA as the dominant or co-dominant immunoglobulin type. The most common histologic manifestation of IgA nephropathy is mesangial proliferative glomerulonephritis (GN), most often focal but not infrequently diffuse. However, the light microscopic appearance of IgA nephropathy spans the entire range from histologically normal to diffuse proliferative and crescentic glomerulonephritis, much as is the case with lupus nephritis. This review examines the histologic diversity as well as the immunohistologic features of IgA nephropathy.     

Asymptomatic haematuria and proteinuria: Renal pathology and clinical outcome in 54 children

In a mass screening programme, 54 children with haematuria and proteinuria were detected and evaluated by clinical findings and renal histology. IgA glomerulonephritis (GN) occurred in 29 patients, diffuse mesangial proliferative GN (DPGN) in 16, membranous GN (MGN) in 4, membranoproliferative GN (MPGN) in 3, and focal segmental glomerular sclerosis (FSGS) was seen in 2. Of the 35 children with proteinuria less than or equal to 1 g/m² per day, 21 with IgA GN and 14 with DPGN had only mild to moderate glomerular changes. None of these children had developed renal impairment after a mean period of 6.5 years (range 5–10 years). On the other hand, 8 children with IgA GN, 2 with DPGN, 4 with MGN, 3 with MPGN, and 2 with FSGS had proteinuria that exceeded 1 g/m² per day. The biopsy specimens from these children showed moderate to severe glomerular changes, and 7 of these children had hypertension or renal impairment during the period of evaluation. This study suggests that a poor outcome correlates with the level of proteinuria and the severity of renal pathology in children with haematuria and proteinuria.     

银屑病合并IgA或非IgA系膜增生性肾小球肾炎六例临床病理分析

目的分析银屑病合并肾损害的临床病理特点。方法回顾性分析北京协和医院1983年至2004年有肾活检结果的银屑病并肾损害患者6例，分析其临床及病理特点。结果男性2例，女性4例，平均年龄38岁。肾损害在银屑病发病后平均16年(7—30年)被发现。2例表现为无症状性镜下血尿和蛋白尿；3例表现为慢性肾炎综合征；1例为肾病综合征。6例均有中大量镜下血尿，其中2例有发作性肉眼血尿：蛋白尿平均为2．05g／24h(0．01—5．42g／24h)；血压4例正常，2例升高；Scr均正常。肾组织免疫荧光检查发现系膜区IgA沉积4例，系膜区IgG沉积1例，免疫荧光阴性1例。光镜表现均不严重，轻度系膜增生3例，中度系膜增生3例；均无新月体形成；慢性肾小管间质病变不明显；2例肾内动脉内膜增生、管腔狭窄。结论在银屑病合并肾损害中，系膜增生性。肾小球肾炎并不少见。可能与银屑病存在一定关系。     

Long-standing spontaneous clinical remission and glomerular improvement in primary IgA nephropathy (Berger's disease)

Of the 244 cases of IgA nephropathy diagnosed at Necker Hospital before 1981, 9 patients (3.7%) developed spontaneous clinical remission of long duration. Three of these 9 patients presented with gross hematuria, while in the others the disease was discovered by the finding of proteinuria at routine urinalysis. During the disease course 5 patients had recurrent episodes of gross hematuria, lasting several years in 4. At the time of the first biopsy all patients had hematuria and permanent proteinuria. In 1 patient, renal biopsy showed only an increase in mesangial matrix while in the others segmentary lesions were observed, affecting less than 30% of the glomeruli in 6. Diffuse mesangial deposits of IgA were present in all. During the follow-up, proteinuria and microscopic hematuria gradually decreased and completely disappeared within 4-14 years after the onset of the disease. A repeat biopsy performed during remission in 4 patients showed, in 3, an improvement of glomerular lesions and a significant decrease in IgA mesangial deposits in parallel with clinical recovery. As in other types of 'primary' glomerulonephritis, these data indicate that the initial disorder in IgA nephropathy may be spontaneously reversible even after a long course of the disease.     

Portions of basement membrane with decreased negative charge in various glomerulonephritis

The decrease in negative charge was evaluated in different portions of the basement membrane as well as the lamina rara externa (LRE) and lamina rara interna (LRI). The subjects were nine patients [2 patients with focal segmental glomerulosclerosis (FGS), 2 with membranoproliferative glomerulonephritis (MPGN), 3 with IgA nephropathy, and 2 with Henoch-Schoenlein purpura nephritis (HSPN)] and 2 patients with minor glomerular abnormalities and 1 with tubulo-interstitial nephritis (TIN) as controls. Polyethyleneimine (PEI) was used as a cationic probe. The basement membrane was divided into the peripheral portion (loop basement membrane 7 microns or more from the anchor portion), proximal portion (within 3 microns of the anchor portion), and the paramesangial portion in the paramesangial basement membrane. In each portion, PEI granules per 1 micron of the LRE and LRI were counted. Anionic sites were decreased in the patients with FGS and MPGN, but the damage pattern differed between the two diseases. In the patients with FGS, the decrease in anionic sites was most marked in the peripheral portion with an even greater decrease in the LRI. In the patients with MPGN, the decrease was uniform among the portions. On the other hand, no significant difference was observed in any portion between the patients with IgA nephropathy or HSPN and the controls. The portions with decreased negative charge varied among various glomerular diseases, suggesting different developmental mechanisms.     

强直性脊柱炎肾损害的临床病理特点

目的探讨强直性脊柱炎（AS）合并肾损害的临床及病理特点。方法回顾性分析18例经肾脏活体组织检查的AS患者的临床及肾脏病理表现。结果18例患者中,9例呈隐匿性肾小球肾炎表现,5例呈慢性肾小球肾炎表现,1例呈肾病综合征表现,3例为慢性肾功能不全;4例血压增高,14例血压正常。24h尿蛋白定量平均为（1．17±1．39）g。15例肾功能正常,3例肾功能异常患者血肌酐平均为（153．2±36．8）umol／L。8例患者血清IgA水平升高,10例c反应蛋白升高,13例红细胞沉降率（EsR）增快,且血清IgA水平和C反应蛋白呈正相关（r=0．707,P=0．001）,血清IgA水平和ESR呈正相关（r=0．858,P〈0．001）。病理检查结果发现15例为IgA肾病（其中10例为轻度系膜增生性肾炎,1例为轻度系膜增生性肾炎并慢性肾小管间质肾病,2例为局灶增生性肾炎,1例为局灶增生坏死性肾炎,1例为局灶节段性肾小球硬化症）,1例为膜性肾病,1例为局灶增生性肾炎伴慢性肾小管间质肾病,1例为慢性。肾小管间质肾病。有慢性肾小管间质肾病者均有服中药史。结论AS相关性肾损伤的病理改变多样,但主要为IgA肾病,也可表现为膜性肾病、局灶增生性肾炎和慢性肾小管间质。肾病,其肾损伤可能与AS疾病本身和（或）治疗用药相关。     

A new morphological classification of urinary erythrocytes for differential diagnosis of glomerular hematuria.

A new morphological classification of urinary erythrocytes was instituted in order to differentiate glomerular from urological hematuria. One hundred and thirteen hematuric patients including 73 glomerular and 40 urological disease patients were examined. The former group consisted of IgA nephropathy (n = 45), lupus nephritis (6), membrano-proliferative glomerulonephritis (5), non-IgA mesangial proliferative glomerulonephritis (4), Henoch-Schoenlein purpura nephritis (4), membranous nephropathy (4), endocapillary proliferative glomerulonephritis (3), and minimal change nephrotic syndrome (2). The latter group included bladder cancer (n = 15), renal calculi (15), prostate cancer (3), urethral cancer (1) and post-transurethral resection (6). In each urine sample, 100 urinary erythrocytes were observed under differential interference microscopy and classified into 10 concretely defined shapes (5 "glomerular" and 5 "urological" shapes) and unclassified shapes. Using percentage of "glomerular" shape erythrocytes and setting the cut-off at 15%, 90.4% of sensitivity and 97.5% of specificity for the diagnosis of glomerular disease were obtained. When percentage of one specific shape (G1), [i.e. doughnut-like cell with one or more blebs] was used at a cut-off of 1%, sensitivity and specificity were 89.0% and 95.0% respectively. These results were satisfactory as compared with most previous reports. Moreover, our classification is so concrete that it is more objective, accurate, and easily understandable, even for beginners. Distinct shape "G1" is particularly important for morphological investigation of hematuria.